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55 publications mentioning hsa-mir-299

Open access articles that are associated with the species Homo sapiens and mention the gene name mir-299. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

1
[+] score: 119
Other miRNAs from this paper: hsa-mir-145, hsa-mir-146a, hsa-mir-146b
microRNA-299-3p downregulates Oct4 expression. [score:6]
d: microRNA-299-3p downregulates promoter activity of Oct4 target. [score:6]
Anti-Oct4-siRNA downregulates Oct4 expression comparable to microRNA-299-3p. [score:6]
c: Mutation of putative binding site of Oct4 3´UTR inhibits down -regulating effect of microRNA-299-3p in comparison to wild type sequence. [score:5]
Compared to murine microRNA expression patterns, the microRNA-299-3p is upregulated in human iPS and native stem cells [34]. [score:5]
These data support the view, that miR-299-3p is a factor which inhibits the expression of stem cell genes like Oct4. [score:5]
miR-299-3p significantly downregulates Oct4 synthesis. [score:4]
In transiently transfected HEK293 cells containing the mutated 3’UTR vector the miRNA-299-3pcould not downregulate the Renilla luciferase anymore. [score:4]
Bioinformatical analysis of targets of human microRNA-299-3p in relation to apoptotic processes (http://www. [score:3]
Thus, it can be concluded, that miR-299-3p not only targets the Oct4 gene transcript, but also many others. [score:3]
org/) analysis of microRNA-299-3p target genes using KEGG database (Kyoto Encyclopedia of Genes and Genomes), in process groups (biological, molecular function, cellular component). [score:3]
High throughput luciferase activity assay revealed the microRNA-299-3p to be the most effective in reducing gene expression of Oct4, which was confirmed by Western blot analysis and Oct4 promoter activity in a target luciferase assay. [score:3]
The results suggest that microRNA-299-3p is an interesting target for potential clinical use. [score:3]
Our results suggest that microRNA-299-3p is an interesting target for potential clinical use. [score:3]
S2 TableBioinformatical analysis of targets of human microRNA-299-3p in relation to apoptotic processes (http://www. [score:3]
A: of malignant illness-related genes using KEGG database (Kyoto Encyclopedia of Genes and Genomes) which are putatively regulated by microRNA-299-3p. [score:2]
If these genes are negatively regulated by miR-299-3p, apoptosis process is facilitated. [score:2]
MicroRNA-299-3p suppresses invasion of mammacarcinoma cells (part II). [score:2]
The comparison of the effect of miR-299-3p and siRNA against Oct4 in invasion and cytotoxic/apoptosis assays reveals the main cause of cell death: It seems that the blocked Oct4 expression leads to cell death initiation, because the application of miR-299-3p and anti-Oct4-siRNA produces similar results. [score:2]
Hence, it may be concluded, that miR-299-3p may be a strong regulator of other central genes apart from Oct4, which are important factors for cell death process. [score:2]
MicroRNA-299-3p suppresses invasion of fibrosarcoma cancer cells (part I). [score:2]
In order to investigate the indirect effect of miR-299-3p on Oct4 targets, a NCC-IT based cell line (DMSZ, Brunswick, Germany, ATCC CRL-2073) with a genomically integrated HIV-derived lentiviral Oct4-reporter construct (Cignal, Qiagen) was transfected with this two microRNAs, and miR -negative control, respectively. [score:2]
The cells were transfected with miR-299-3p and negative control. [score:1]
Therefore, we analyzed the human anti-Oct4 microRNA-299-3p and in invasion experiments. [score:1]
In HT-1080 cells, the microRNA-299-3p nearly completely blocked invasion as seen above. [score:1]
The microRNA-299-3p is less mentioned in the literature at present. [score:1]
This is not true for the non-cancer cells (Fig 6b and 6d); hence, it is quite probable, that miR-299-3p acts via Oct4 and related genes. [score:1]
d: microRNA-299-3p decreases number of invasion events of MDA-MB-231 breast cancer cells. [score:1]
0174912.g006 Fig 6 a: The microRNA-299-3p is toxic to breast cancer cells (MDA-MB-231). [score:1]
The day before highly invasive breast carcinoma cells (MDA-MB-231, ACC-732 by DMSZ, via lab JHC and clinic for women’s health, Jena) were transfected with microRNA-299-3p, miR -negative control, siRNA against Oct4 and AGTR1 (150 pmol and 400,000 cells per well in a 6-well cell culture plate, siRNA as above). [score:1]
HT-1080-cells transfected with pre-microRNA-scramble (negative control, 1) and -299-3p (2), Cells with microRNA-299-3p show a decreased invasive behavior in relation to negative control, False colors images. [score:1]
a: microRNA-299-3p completely avoids branching of invasive MDA-MB-231 breast cancer cells. [score:1]
org) revealed some genes controlled by miR-299-3p which are connected to apoptosis. [score:1]
b and c: Oct4 protein production is decreased by microRNA-299-3p in NCC-IT cells. [score:1]
Additionally, microRNA-299-3p causes apoptosis in cancer cells. [score:1]
a: Decreased invasive behavior of HT-1080 cells caused by transfection with microRNA-299-3p (fluorescence sample images). [score:1]
B: of putatively miR-299-3p influenced pathways using KEGG database (Kyoto Encyclopedia of Genes and Genomes). [score:1]
d: microRNA-299-3p completely avoids branching of of HT-1080 fibrosarcoma cells. [score:1]
0174912.g004 Fig 4 a: Decreased invasive behavior of HT-1080 cells caused by transfection with microRNA-299-3p (fluorescence sample images). [score:1]
In Western blots the Oct4 protein (isoform A) was quantified in NCC-IT-Oct4 cells which were transfected with microRNA-299-3p (and negative control, respectively, see Fig 2b and 2c). [score:1]
The predicted hybridization site of microRNA-299-3p was located at base position 200–206 of the Oct4 3’UTR. [score:1]
a: The microRNA-299-3p is not toxic to HT-1080 fibrosarcoma cells. [score:1]
The microRNA-299-3p seems to be effective in inducing cell death, more specifically, apoptosis. [score:1]
Binding sites of microRNA-299-3p in 3’UTR of Oct4. [score:1]
Breast cancer cells (MDA-MB-231) and fibrosarcoma cells (HT-1080) transfected with microRNA-299-3p (and unstimulated as negative control, respectively) were seeded in cell culture chips, which were already filled with dyed Matrigel. [score:1]
b: Decreased invasive behavior of mammacarcinoma cells caused by transfection with microRNA-299-3p(fluorescence sample images). [score:1]
Cells with microRNA-299-3pshow an extremely decreased invasive behavior in relation to negative control. [score:1]
This might lead to the toxic effect we could observe in MDA-MB-231 and HT-1080 cells transfected with miR-299-3p. [score:1]
a: The microRNA-299-3p is toxic to breast cancer cells (MDA-MB-231). [score:1]
The bioinformatically predicted hybridization site of miRNA-299-3p could thus be confirmed. [score:1]
The microRNA-299-3p causes cell death in breast cancer cells, but not in non-cancer cells. [score:1]
b: Evolutionary conservation of microRNA-299-3pbinding sites in human Oct4 gene on chromosome 6. Site for 299-3p is poorly conserved. [score:1]
b: The microRNA-299-3p causes apoptosis in HT-1080 fibrosarcoma cells. [score:1]
On the contrary, the miR-299-3p seems to have evolved its function as a repressor of Oct4 much later at the level of primates. [score:1]
This view is supported by the fact, that miR-299-3p is more toxic to breast cancer cells than anti-Oct4-siRNA. [score:1]
Cells transfected with microRNA-299-3p showed a decrease of Firefly luciferase signal in comparison to controls (see Fig 2d). [score:1]
To investigate what area of the Oct4 3 'UTR is bound by effective microRNAs (miR299-3p), the putative binding sites were determined using the bioinformatical service TargetScan (www. [score:1]
Object lense: 10x /1,2,; 40x/ 3. c: microRNA-299-3p decreases invasion distance of MDA-MB-231 breast cancer cells. [score:1]
However, in HT1080 cells, the miR-299-3p was not toxic. [score:1]
The miR-299-3p was toxic and clearly induced apoptosis in cancer cells; so does siRNA against Oct4 (Figs 6a, 6c and 7). [score:1]
c: The microRNA-299-3p causes apoptosis in breast cancer cells (MDA-MB-231). [score:1]
In MDA-MB-231 cells, the microRNA-299-3p transfected cells lost their invasiveness almost completely (Figs 3c and 3d, 5a and 4b to 4d). [score:1]
It was found that the binding sequence of miR-299-3p is located in an only moderately conserved region (see Fig 1b). [score:1]
0174912.g005 Fig 5 a: microRNA-299-3p completely avoids branching of invasive MDA-MB-231 breast cancer cells. [score:1]
0174912.g007 Fig 7 a: The microRNA-299-3p is not toxic to HT-1080 fibrosarcoma cells. [score:1]
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2
[+] score: 51
To assess whether miRNA with expression divergence on the human lineage might be associated with human cognitive functions, we investigated the expression of genes targeted by five miRNA showing human-specific expression, according to multiple methodologies: miR-184, miR-487a, miR-383, miR-34c-5p and miR-299-3p (Figure 2). [score:7]
Potential influence of miRNA divergence on neuronal functions was further confirmed by preferential expression of the corresponding miR-299-3p and miR-184 in cortical neurons, as well as verification of the predicted miRNA-target relationship in two human neuroblastoma cell lines. [score:5]
While this substitution might affect relative stand selection efficiency during miRNA procession, as well as target selection, we did not find any significant differences in target effects between the human and the chimpanzee versions of miR-299-3p in our experiment (Figure S8). [score:5]
The X and Y-axis show the target effect produced by hsa-miR-299-3p and ptr-miR-299-3p transfection, respectively. [score:3]
To further test association of miR-184 and miR-299-3p with neuronal functions, we determined their expression patterns in the human and macaque prefrontal cortex by in situ hybridization with specific LNA-probes (Table S11). [score:3]
Similarly, targets of miR-299-3p were significantly enriched in the “axon guidance” pathway, which is associated with neuronal cell differentiation and functions. [score:3]
Similarly, based on the DIANA-mirPath algorithm [33], targets of miR-184, miR-487a and miR-299-3p were significantly enriched in KEGG pathways that are related to neural functions (Table S10). [score:3]
Requiring significant support by at least two out of three methodologies (sequencing, microarrays and Q-PCR), expression changes in five miRNA (miR-184, miR-299-3p, miR-487a, miR-383 and miR-34c-5p) could be assigned to the human evolutionary lineage and two (miR-375 and miR-154*) to the chimpanzee evolutionary lineage (Figure 2). [score:3]
We tested the effects of all five miRNA showing human-specific expression in brain, as well as effects of the chimpanzee version of miR-299-3p sequence. [score:3]
Further, in both cell lines we observed highly correlated target effects after transfection with human and chimpanzee versions of miR-299-3p. [score:3]
Figure S8 Target effects of human and chimpanzee variants of miRNA 299-3p (hsa-miR-299-3p and ptr-miR-299-3p) after transfection in two cell lines. [score:3]
Based on the DIANA-mirPath algorithm, targets of miR-184, miR-487a and miR-299-3p were significantly enriched in KEGG pathways that are related to neural functions (Table S10). [score:3]
The red legend in the bottom right corner of each plot shows the Pearson correlation coefficient of target effect between hsa-miR-299-3p transfection and ptr-miR-299-3p transfection into SH-SY5Y (panel A) and SK-N-SH (panel B) cell lines, calculated using Mock 1 as a negative control (R) and the correlation p-value (p). [score:1]
1002327.g004 Figure 4 In situ staining of miR-184 and miR-299-3p in prefrontal cortex. [score:1]
In situ staining of miR-184 and miR-299-3p in prefrontal cortex. [score:1]
On the DNA sequence level, these miRNA tend to be conserved: miR-184 mature miRNA sequence is evolutionarily conserved from insects to humans, with only one nucleotide different at 3′end of mature sequence, while miR-383 and miR-34c-5p are classified as broadly conserved and miR-299-3p - as conserved among animal species [25], [31]. [score:1]
We designed two LNA-probes complementary to miR-184 and miR-299-3p respectively (Table S11). [score:1]
We chose three types of miRNA differences: (1) consistent by both methodologies: miR-383 and miR-34c-5p; (2) significant according to sequencing, but unconfirmed in the microarray experiment: miR-143 and miR-499; (3) significant according to sequencing, but not detected or masked on the microarrays: miR-184 and miR-299-3p. [score:1]
The mature sequence of miR-299-3p contains human-specific C to T substitution at position 10. [score:1]
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3
[+] score: 49
Other miRNAs from this paper: hsa-mir-34a, hsa-mir-211, hsa-mir-216b
The results showed that patients with higher miRNA expression levels in EC tissue displayed substantial down-regulation of VEGFA (R [2] = 0.43, P < 0.05 for miR-299; R [2] = 0.48, P < 0.05 for miR-34a-5p; Figure 2E). [score:6]
In our lncRNA-TUG1 knockdown cells, the expression level of VEGFA was significantly reduced in the presence of miR-299 and miR-34a-5p, suggesting that lncRNA-TUG1 may functions as a ceRNA to regulate VEGFA levels by sponging miRNA. [score:5]
Past researchers have found that overexpression of miR-299 could suppress the proliferation of metastatic prostatic cancer cells [32]. [score:5]
Through a series of experiments, we concluding that lncRNA-TUG1 act as one competitive endogenous RNAs (ceRNA) negative regulate the miR-299 and miR-34a-5p and influence the expression of VEGFA in EC. [score:4]
In our study, we verified the roles of miR-299 and miRNA-34a in endometrial cancer progression, the results of dual-luciferase reporter assay show that both two miRNAs could direct regulate VEGFA expression in EC cells. [score:4]
lncRNA-TUG1 regulates VEGFA expression by competing for miR-299 and miR-34a-5p. [score:4]
Coincidentally, the miR-299 and miR-34a-5p was the experimental verified target for both lncRNA-TUG1 and VEGFA [14, 17]. [score:3]
lncRNA-TUG1 and VEGFA are targeted by miR-299 and miR-34a-5p. [score:3]
LncRNA-TUG1 may improve VEGFA expression by competing for miR-299 and miR-34a-5p, subsequently mediating cell proliferation in EC. [score:3]
Aberrant expression of miR-299 was determined in various kind of cancers, such as breast cancer and metastatic prostate cancer [31]. [score:3]
E. The linear correlations between the miR-299 and miR-34a-5p expression levels and VEGFA mRNA were tested. [score:3]
Identically, there was a reciprocal repression between lncRNA-TUG1 and miR-299, lncRNA-TUG1-miR-299 constitutes a ceRNA regulatory network in the progress of glioblastoma. [score:2]
Coincidentally, our data also affirmed that lncRNA-TUG1 forms a molecular decoy for miR299 and miR-34a-5p in EC cells. [score:1]
The results showed that both miR-299 and miR-34a-5p significantly decreased the luciferase signals of the mentioned reporters above (Figure 3A, B). [score:1]
To test the role of miR-299 and miR-34a-5p in the EC cells, the 3′ UTR of VEGFA and TUG1 cDNA was cloned into the downstream of luciferase gene and transfected into EC cells with miR-299 and miR-34a-5p mimics respectably. [score:1]
The predict potential binding sites of lncRNA-TUG1 and 3′UTR of VEGFA with miR-299 and miR-34a-5p were showed in Figure 3E. [score:1]
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4
[+] score: 48
Interestingly, MFE differences between the human and non-human hairpins of mir-299, mir-508 and mir-541 were in accordance with the differential expression levels observed between variants: more expressed variants showed higher stabilities and pairs of miRNA variants with stronger expression differences showed larger MFE differences. [score:7]
Specifically, the non-human versions of miR-299-3p and miR-541-3p were four and one and a half times more expressed than the human miRNAs respectively, whereas human miR-508-3p was seven times more expressed than the non-human version. [score:5]
Moreover, genes deregulated by miR-299-3p and miR-541-3p were involved in reproductive and infectious diseases and non-human miR-503-3p, human miR-508-3p and both variants of miR-541-3p were associated with neurological disorders. [score:4]
We found expression of miR-299-3p in brain, placenta and testis in all the studied primates and mouse. [score:3]
Remarkably, non-human miR-299-3p regulated genes with important roles in nervous system development and function. [score:3]
We next centered our interest in the analysis of the expression of four miRNAs with human-specific substitutions located either in the mature (miR-299-3p, miR-508-3p and miR-541-3p) or in the seed regions (miR-503-3p). [score:3]
On one hand, miR-299-3p and miR-541-3p change the expression of a large number of genes (between one and two thousands genes). [score:3]
In accordance we observed a significant expression of miR-299-3p and miR-541-3p in brain tissues from different primates. [score:3]
Remarkably, miR-299-3p was highly amplified in cerebellum but poorly detected in other brain regions whereas miR-508-3p and miR-541-3p were expressed in several regions such as hypothalamus, hippocampus, frontal, parietal and temporal cortex. [score:3]
The human and non-human versions of miR-299-3p and miR-541-3p deregulated more than one thousand genes, while both versions of miR-503-3p and miR-508-3p deregulated less than 300 genes. [score:3]
Human miR-299-3p and miR-541-3p deregulated about the 10% of the genes in an exclusive manner, but these proportions reached about 50% for human miR-503-3p and miR-508-3p. [score:2]
For expression level analyses, pre-miRNA genomic sequences of the selected miRNAs (mir-299, mir-503, mir-508 and mir-541) and ~100 bp flanking regions at each side were PCR amplified (primers in S2 Table). [score:2]
We have thoroughly studied the possible functional consequences of human-specific substitutions in the mature region of four miRNAs and show that miR-299-3p and miR-541-3p are conserved miRNAs with neuronal functions and thus evolutionary changes in these miRNAs may have had an impact in gene regulatory networks ultimately related to the evolution of the nervous system. [score:2]
We suggest that this could be the case for mir-299 and mir-508 for which the hairpin length between humans and the other great apes has been described to be different. [score:1]
For transcriptome analyses SH-SY5Y cells were transfected with 100 μM of miRNA mimic variants (miR-299-3p, miR-503-3p, miR-508-3p, miR-541-3p or the related negative control) as previously described [38]. [score:1]
After discarding polymorphism changes (1000 Genomes database) [34], four miRNA candidates were studied: miR-503-3p, with a single human-specific nucleotide substitution in the seed region, and miR-299-3p, miR-508-3p and miR-541-3p with human-specific nucleotide substitutions in the mature out of the seed region (Table 1). [score:1]
Besides nucleotide substitutions, precursor molecules of the human and non-human versions of mir-299 and mir-508 described in miRBase also differ in length (Fig 6). [score:1]
In addition, changes in the hairpin stabilities of mir-299 and mir-508 could also be affected by changes in the precursor molecule lengths. [score:1]
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5
[+] score: 31
Four differentially expressed miRNAs (including miR-203, miR-299-5p, miR-885-5p, and miR-320c) were predicted to participate in Wnt signaling pathway through regulating their potential gene targets. [score:6]
0114627.g005 Figure 5 Four differentially expressed miRNAs (including miR-203, miR-299-5p, miR-885-5p, and miR-320c) were predicted to participate in Wnt signaling pathway through regulating their potential gene targets. [score:6]
0114627.g002 Figure 2. TaqMan real-time RT-PCR to validate the expression levels of nine up regulated miRNAs, including let-7a, miR-199b, miR-218, miR-148a, miR-135b, miR-203, miR-219, miR-299-5p, and miR-302b (A) and three down regulated miRNAs, including miR-885-5p, miR-181a, and miR-320c (B) from miRNA array were selected for further validation using individual exosomal samples from BMSCs when cultured at 0, 0.5, 1, 1.5, 2, 2.5, 3, 4, 5, 7 days. [score:5]
TaqMan real-time RT-PCR to validate the expression levels of nine up regulated miRNAs, including let-7a, miR-199b, miR-218, miR-148a, miR-135b, miR-203, miR-219, miR-299-5p, and miR-302b (A) and three down regulated miRNAs, including miR-885-5p, miR-181a, and miR-320c (B) from miRNA array were selected for further validation using individual exosomal samples from BMSCs when cultured at 0, 0.5, 1, 1.5, 2, 2.5, 3, 4, 5, 7 days. [score:5]
0114627.g003 Figure 3 Four differentially expressed miRNAs (including miR-203, miR-299-5p, miR-885-5p, and miR-320c) were selected as examples for examining miRNA-mRNA relationships in RNA degradation. [score:3]
Nine up regulated miRNAs (let-7a, miR-199b, miR-218, miR-148a, miR-135b, miR-203, miR-219, miR-299-5p, and miR-302b) and five down regulated miRNAs (miR-221, miR-155, miR-885-5p, miR-181a, and miR-320c) from miRNA array were selected for further validation using individual exosomal samples from BMSCs when cultured at 0, 0.5, 1, 1.5, 2, 2.5, 3, 3.5, 4, 4.5, 7 days. [score:3]
nine up regulated miRNAs (let-7a, miR-199b, miR-218, miR-148a, miR-135b, miR-203, miR-219, miR-299-5p, and miR-302b) and five down regulated miRNAs (miR-221, miR-155, miR-885-5p, miR-181a, and miR-320c) from miRNA array were further quantitated by TaqMan miRNA assays (Applied Biosystems). [score:2]
Furthermore, we found that let-7a, miR-199b, miR-218, miR-148a, miR-135b, miR-203, miR-219, miR-299-5p, and miR-302b were significantly increased in individual exosomal samples from human BMSCs. [score:1]
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6
[+] score: 25
While expression of some of these miRNAs seemed to be specifically dysregulated in certain tumor stages, 12 miRNAs, including 4 up-regulated (miR-200c, miR-487a, miR-491-3p and miR-452) and 8 down-regulated miRNAs (miR-125b, miR-142-3p, miR-199a-5p, miR-22, miR-299-3p, miR-29a, miR-429, and miR-532-5p), were identified to be commonly dysregulated in all ccRCC tumors at different stages (Table 1). [score:11]
Eleven miRNAs were identified to be commonly dysregulated, including three up-regulated (miR-487a, miR-491-3p and miR-452) and eight down-regulated (miR-125b, miR-142-3p, miR-199a-5p, miR-22, miR-299-3p, miR-29a, miR-429, and miR-532-5p) in tumor tissues as compared with adjacent normal tissues. [score:7]
Eleven commonly dysregulated miRNAs, including 3 up-regulated (miR-487a, miR-491-3p and miR-452) and 8 down-regulated (miR-125b, miR-142-3p, miR-199a-5p, miR-22, miR-299-3p, miR-29a, miR-429, and miR-532-5p), were identified in ccRCC tumor samples as compared with adjacent nontumorous samples. [score:7]
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7
[+] score: 24
The double-stranded oligonucleotides encoding the pre-miRNA sequences of miR-376a, miR-299, miR-382 or irrelevant miRNA (a miR -negative control, predicted not to target any known vertebrate gene) were cloned into the pcDNA6.2-GW/EmGFP-miR expression vector such that the pre-miRNA insertion site was in the 3′ untranslated (3′UTR) region of the green fluorescent protein (GFP) gene as per the instruction manual (Invitrogen, Carlsbad, CA). [score:7]
0014416.g004 Figure 4 (A) of stably expressing miR-376a, miR376abc (a polycistronic cluster of miR-376a, miR-376b and miR-376c), miR-299-5p or miR -negative and 10-87 LP cells; (B) with stably expressing miR-376a, miR-376abc, miR-299-5p or miR -negative 10-87 HP cells. [score:5]
No change in migration and invasion phenotypes was observed in cells expressing miR-382 or miR-299-5p. [score:3]
To determine whether the overexpression of the identified signature miRNAs could confer phenotypic changes, stable cell lines were created by cloning the pre-miRNA sequences of miR-376a, miR-376abc, miR-299, or miR-382 into the pcDNA6.2-GW/EmGFP-miR vector, which contains a green fluorescent protein (GFP) cassette, and introducing them into the non-tumorigenic 10-87 LP cells. [score:3]
However, little or no migration was observed for cells expressing miR-299 or miR-382. [score:3]
In agreement with the wound-healing assay, over -expression of miR-376a or miR-376abc also resulted in more than a four-fold increase in invasiveness, whereas miR-299 or miR-382 had no effect (Fig. 4B). [score:2]
miR-299-5p sense, 5′- tgctGAAGAAATGGTTTACCGTCCCACATACATTTTGAATATGTATGTGGGATGGTAAACCGCTTCTT-3′ and miR-299-5p anti-sense 5′-cctgAAGAAGCGGTTTACCATCCCACATACATATTCAAAATGTATGTGGGACGGTAAACCATTTCTTC-3′, miR-382 sense 5′- tgctGTACTTGAAGAGAAGTTGTTCGTGGTGGATTCGCTTTACTTATGACGAATCATTCACGGACAACACTTTTTTCAGTA-3′ and miR-382 anti-sense 5′-cctgTACTGAAAAAAGTGTTGTCCGTGAATGATTCGTCATAAGTAAAGCGAATCCACCACGAACAACTTCTCTTCAAGTAC-3′. [score:1]
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8
[+] score: 21
For example, upregulated miRNAs targeted CDC7 (targeted by miR-30a-5p and miR-630) and CDK2 (targeted by miR-638), while downregulated miRNAs targeted CDKN1A (targeted by miR-299-5p), CDKN1B (targeted by miR-218-5p and miR-495-3p) and CCNA2 (targeted by miR-218-5p). [score:21]
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9
[+] score: 20
MiR-299 was found down-regulated in prostatic cancer cell lines compared to normal cells [17] and to play a role in autophagy inhibition by suppressing Atg5 in neurons [18]. [score:6]
The expression levels of miRNAs were ranked according to BH values and the top five significant miRNAs were: miR-337-3p, miR-185-5p, miR-485-3p, miR-197-3p, and miR-299-5p, all down-regulated in MPM. [score:6]
We observed a statistically significant down-regulation in MPM samples, after Bonferroni’s correction, for miR-197, miR-185 and miR-299 (see Table  1), whereas we could not validate the results for miR-337 and miR-485. [score:4]
Thus, overall, we confirmed the role played by miR-126, miR-15b and miR-145 and, in addition, we suggest a role for miR-185, miR-197, and miR-299 in MPM. [score:1]
microRNALog [2](FC) p-value miR-197-3p −2.540 3.72 × 10 [−7] miR-185-5p −2.742 2.22 × 10 [−4] miR-299-5p −1.239 0.0014 miR-337-3p −0.758 0.0201 miR-485-3p −0.488 0.1886 In addition, from our microarray analysis we could confirm previous findings from several high-throughput studies where mesothelial cell lines or normal mesothelial tissues were used as controls (Table  2). [score:1]
This approach allowed the identification of six miRNAs (miR-15b, miR-126, miR-145, miR-185, miR-197, and miR-299), three of which (i. e. miR-185, miR-197 and miR-299) have never been linked, to the best of our knowledge, to MPM carcinogenesis. [score:1]
microRNALog [2](FC) p-value miR-197-3p −2.540 3.72 × 10 [−7] miR-185-5p −2.742 2.22 × 10 [−4] miR-299-5p −1.239 0.0014 miR-337-3p −0.758 0.0201 miR-485-3p −0.488 0.1886 In addition, from our microarray analysis we could confirm previous findings from several high-throughput studies where mesothelial cell lines or normal mesothelial tissues were used as controls (Table  2). [score:1]
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10
[+] score: 17
Our study also identified miR-107 and miR-299-3p as being responsible for an up-regulation in the expression of human GP Ibα mRNA. [score:6]
Furthermore, by performing a literature review, we found that miR-10a, miR-10b and miR-107 were previously reported to be involved in the regulation of hematopoietic gene expression [15, 19], and miR-299-3p is predicted to target the 3′-UTRs of both human and mouse GP1BA gene. [score:6]
Therefore, we chose to assess four miRNAs (miR-10a, miR-10b, miR-107, and miR-299-3p) and investigate if they can target the 3′-UTR and regulate the expression of human GP Ibα (Figure 1A). [score:4]
Of these two miRNAs, interestingly, miR-299-3p is predicted to bind the 3′-UTRs of both human and mouse GP1BA gene and thus is potentially able to play important roles in GP Ibα expression and megakaryopoiesis in both human and mouse, a speculation worthy of further investigations. [score:1]
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11
[+] score: 15
Two other down-regulated miRNAs, miR-299-3p and miR-381-3p, are predicted to suppress expression of integrin V (ITGAV) (Table 2 and Fig 6), which was in turn up-regulated in SLKK cells. [score:11]
Interestingly, miR-409-5p, miR-299-3p, and miR-381-3p are all located in the 14q32 cluster that is broadly down-regulated in SLKK cells as well as PEL cells [33]. [score:4]
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12
[+] score: 13
Other miRNAs from this paper: hsa-mir-4513
The in PBC over-expressed hsa-mir-299-5p is hypothesized to target SMC4 at the seed complementary region where rs10923 is located. [score:5]
The SNP rs10923 is localized within an experimentally validated RISC binding site [14] and lies directly in the seed complementary region of hsa-mir-299-5p, a miRNA that has been shown to be up-regulated in PBC patients [46]. [score:5]
With the major allele, SMC4 is silenced, whereas the mutated SMC4-G cannot be bound by hsa-mir-299-5p and therefore is translated without interference. [score:3]
[1 to 20 of 3 sentences]
13
[+] score: 12
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-let-7c, hsa-let-7d, hsa-let-7e, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-15a, hsa-mir-16-1, hsa-mir-17, hsa-mir-21, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-26a-1, hsa-mir-26b, hsa-mir-27a, hsa-mir-29a, hsa-mir-30a, hsa-mir-98, hsa-mir-101-1, hsa-mir-29b-1, hsa-mir-29b-2, hsa-mir-106a, hsa-mir-107, hsa-mir-16-2, hsa-mir-198, hsa-mir-148a, hsa-mir-30d, hsa-mir-7-1, hsa-mir-7-2, hsa-mir-7-3, hsa-mir-34a, hsa-mir-181a-2, hsa-mir-181c, hsa-mir-182, hsa-mir-183, hsa-mir-205, hsa-mir-210, hsa-mir-181a-1, hsa-mir-222, hsa-mir-224, hsa-mir-200b, hsa-let-7g, hsa-let-7i, hsa-mir-23b, hsa-mir-27b, hsa-mir-124-1, hsa-mir-124-2, hsa-mir-124-3, hsa-mir-125b-1, hsa-mir-128-1, hsa-mir-132, hsa-mir-137, hsa-mir-140, hsa-mir-141, hsa-mir-142, hsa-mir-143, hsa-mir-144, hsa-mir-153-1, hsa-mir-153-2, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-125a, hsa-mir-125b-2, hsa-mir-126, hsa-mir-134, hsa-mir-136, hsa-mir-146a, hsa-mir-150, hsa-mir-184, hsa-mir-185, hsa-mir-186, hsa-mir-206, hsa-mir-320a, hsa-mir-200c, hsa-mir-128-2, hsa-mir-200a, hsa-mir-101-2, hsa-mir-34b, hsa-mir-34c, hsa-mir-26a-2, hsa-mir-373, hsa-mir-376a-1, hsa-mir-342, hsa-mir-133b, hsa-mir-424, hsa-mir-429, hsa-mir-433, hsa-mir-451a, hsa-mir-146b, hsa-mir-494, hsa-mir-193b, hsa-mir-455, hsa-mir-376a-2, hsa-mir-33b, hsa-mir-644a, hsa-mir-548d-1, hsa-mir-548d-2, hsa-mir-320b-1, hsa-mir-320c-1, hsa-mir-320b-2, hsa-mir-301b, hsa-mir-320d-1, hsa-mir-320c-2, hsa-mir-320d-2, hsa-mir-320e, hsa-mir-3613, hsa-mir-4668, hsa-mir-4674, hsa-mir-6722
It is demonstrated that miRNA-299-5p regulates autophagy by targeting ATG 5 directly (Zhang et al., 2016). [score:5]
miRNA-299-5p downregulation is observed in APPswe/PS1dE9 mice, cerebrospinal fluid of AD patients, N2a and SH-SY5Y cell mo dels of the AD. [score:4]
miRNA-299-5p plays a crucial role in AD pathogenesis by regulating apoptosis through autophagy in N2a and SH-SY5Y cells and a mouse mo del of the AD (Zhang et al., 2016). [score:2]
MiR-299-5p regulates apoptosis through autophagy in neurons and ameliorates cognitive capacity in APPswe/PS1dE9 mice. [score:1]
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14
[+] score: 11
Xing Y. Cui D. Wang S. Wang P. Xing X. Li H. Oleuropein represses the radiation resistance of ovarian cancer by inhibiting hypoxia and microRNA-299-targetted heparanase expressionFood Funct. [score:7]
In a study where human ovarian cancer cell lines were used for xenograft assay and were irradiated and treated with 200 µM of OLE, the treatment altered the miR expression profile, specifically; the endogenous expression of miR-299 was repressed by a hypoxia inducible factor and reassured with OLE treatment [208]. [score:4]
[1 to 20 of 2 sentences]
15
[+] score: 10
com), hsa-miR-299-5p has been reported to target OPN and regulate the expression of OPN 34. miRNA 181a targets OPN and decreases OPN expression in hepatocellular cancer cell lines (Hep 3B and Hep G2) 35, vascular smooth muscle cells 36. [score:10]
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16
[+] score: 9
Our findings also demonstrate that miR-299, miR-499, miR-302, and miRNA-200 were upregulated in EPO-MVs (Fig.   8c). [score:4]
The miRNA profiles of the MVs revealed that EPO-MVs changed 212 miRNAs (fold-change ≥ 1.5), including miR-299, miR-499, miR-302, and miRNA-200, and that 70.28 % of these changes involved upregulation. [score:4]
miR-299 may delay or protect against replicative senescence via improvements in the metabolic activity of senesced cells, but it does not stimulate growth in the remaining senescent cells [46]. [score:1]
[1 to 20 of 3 sentences]
17
[+] score: 8
12 microRNAs passed the threshold of mean fold change > 1.3 and p-value < 0.05 between the lean and obese groups, with one microRNA significantly downregulated (miR-299-3p) and nine significantly upregulated (miR-202-3p, -15b-5p, -451, -24-2-5p, 1184, -187-5p, -486-5p, -10b-5p, and -223-3p). [score:7]
miR-187, miR-202, and miR-299-3p were not significantly correlated with any of the four markers. [score:1]
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18
[+] score: 8
Interestingly, similar to what has been found in porcine muscle development, miR-299–5p was up-regulated during human muscle development. [score:6]
In contrast, miR-1, miR-299–5p, miR-381, miR-193b* and let-7a seem to be more associated with the third phase of muscle development, the volumetric growth and maturation of the muscle fibers (Stg3, Fig. 3B). [score:2]
[1 to 20 of 2 sentences]
19
[+] score: 7
In the cases of miR-130b and miR-19a, up regulated in HP (with positive correlation with the cell-cycle genes), and miR-449a, miR-299, miR-154 and miR-145, downregulated in HP (with negative correlation with the cell-cycle genes), the effect of miRNA over -expression on proliferation was confirmed in cell lines. [score:7]
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20
[+] score: 7
Localized on chromosome 14q101, miR-299-3p was recently proposed to be part of a miRNA signature that predicts estrogen receptor expression in breast cancer patients, indicating that this miRNA may play a role in hormonal regulation in normal tissues and during oncogenesis [47]. [score:4]
Consistent with this idea, three-way analysis of variance analysis using sex, race and age as variables revealed that only miR-299-3p was significantly altered in different sexes, expression is lower in males than females (data not shown). [score:3]
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21
[+] score: 7
The miRNA signatures generated for ER status (miR-342, miR-299, miR-217, miR-190, miR-135b, miR-218), for PR status (miR-520g, miR-377, miR-527-518a, miR-520f-520c) and for HER2/ neu status (miR-520d, miR-181c, miR-302c, miR-376b, miR-30e) include miRNAs that have previously been identified as dysregulated in breast cancer and other cancers [7, 9, 37- 43] and involved in the regulation of cell functions such as growth, apoptosis, migration and invasion [38, 42, 43]. [score:3]
Notably, two chromosomal locations account for a number of the dysregulated miRNAs in these predictive sets: Ch19q13 (miR-520g, miR-520d, miR-527-528a, miR-520f-520c, miR-181c) and Ch14q32 (miR-342, miR-299, miR-377, miR-376b). [score:2]
The ER signature consisted of six miRNA transcripts (miR-342, miR-299, miR-217, miR-190, miR-135b, miR-218), and discriminated cases correctly with a median accuracy of 100% when classifying between ER -positive and ER -negative phenotypes. [score:1]
Stepwise ANN analysis identified predictive miRNA signatures corresponding with oestrogen (miR-342, miR-299, miR-217, miR-190, miR-135b, miR-218), progesterone (miR-520g, miR-377, miR-527-518a, miR-520f-520c) and HER2/ neu (miR-520d, miR-181c, miR-302c, miR-376b, miR-30e) receptor status. [score:1]
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22
[+] score: 7
Our newly identified ES/iPS cell-specific miRNAs, miR-299, -499-5p, -628-5p, and -888, were included in the list, further confirming that these miRNAs are more highly expressed in immature cells than in differentiating or differentiated cells. [score:3]
However, the involvement of miR-187, miR-299-3p, and miR-628-5p in some aspects of biology, including cancer, has been reported [43]– [46]; thus these miRNAs may play roles in regulating the proliferation of iPS/ES cells. [score:2]
However, a previous microarray study did not detect miR-299-3p in ES or iPS cells, perhaps because of the insensitivity of the microarray technique used [13]. [score:1]
miR-299-3p was described in ESCs [31], but not in iPSCs. [score:1]
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23
[+] score: 6
In [47] a predominant upregulation has been shown for miR-370, miR-299 and miR-125b which putatively affects the expression of BAX/AKT, β-catenin, IGF R type I, respectively. [score:6]
[1 to 20 of 1 sentences]
24
[+] score: 6
Unfortunately, we could not detected miR-299-5p, possibly because only a small amount was expressed. [score:3]
However, we could not determine the changes in miR-1469 because no TaqMan miRNA assay kit was available; nor miR-299-5p, possibly because it was only expressed at low levels. [score:2]
Based on the criteria described in the Method (fold-change >1.5, coefficient of variation <50%, and high Hy3 signal >1.5× the median signal), only four miRNAs (miR-149*, miR-299-5p, miR-1469 and miR-1908) were selected. [score:1]
[1 to 20 of 3 sentences]
25
[+] score: 6
Cai H, Liu X, Zheng J, Xue Y, Ma J, Li Z, Xi Z, Li Z, Bao M, Liu Y 2017 Long non-coding RNA taurine upregulated 1 enhances tumor -induced angiogenesis through inhibiting microRNA-299 in human glioblastoma. [score:6]
[1 to 20 of 1 sentences]
26
[+] score: 6
Other miRNAs from this paper: hsa-mir-940
Long non-coding RNA taurine upregulated 1 promotes tumor -induced angiogenesis by inhibiting microRNA-299 in human glioblastoma [30]. [score:6]
[1 to 20 of 1 sentences]
27
[+] score: 6
detected the expression profile of miRNAs from blood samples of influenza A H1N1 virus-infected patients and then exhibited that the expression levels of 193 miRNA molecules were altered in all influenza patients, of which 16 highly dysregulated miRNAs (miR-1260, miR-1285, miR-18a, miR-185*, miR-299-5p, miR-26a, miR-30a, miR-335*, miR-34b, miR-519e, miR-576-3p, miR-628-3p, miR-664, miR-665, miR-765 and miR-767-5p) were able to provide a clear distinction between infected and healthy individuals [39]. [score:6]
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28
[+] score: 6
Four additional miRNAs, miR-299, miR-182, miR-23a and miR-125b, representing varying degrees of differential expression were validated using. [score:3]
miR-299, miR-182, miR-23a and miR-125b are representative of varying degrees of differential expression in the array. [score:3]
[1 to 20 of 2 sentences]
29
[+] score: 5
Other miRNAs from this paper: hsa-mir-567, hsa-mir-609, hsa-mir-297, oar-mir-299
miRNA, such as miRNA-297, miRNA-299, miRNA-567 and miRNA-609 are able to control its expression by preventing protein production without inhibition of the transcription [28]. [score:5]
[1 to 20 of 1 sentences]
30
[+] score: 5
Except novel-miR-299-5p, which was not expressed in 2 samples (pre-feed milk sample 6, and post-feed milk sample 3), all other 3 novel miRNAs tested were expressed at high levels in all samples (Figure 2). [score:5]
[1 to 20 of 1 sentences]
31
[+] score: 5
For the efficient targets CD27, TLR7 and TNFAIP3, miR-299-3p, miR-525-5p and miR-603 repressed them only in CIN I stage, respectively, and these targets have contribution to the processes of ‘immunoglobulin mediated immune response’, ‘release of cytoplasmic sequestered NF-kappaB’, ‘pathogen - associated molecular pattern dependent induction by symbiont of host innate immune response’, and ‘response to molecule of bacterial origin’ only in CIN III stage. [score:5]
[1 to 20 of 1 sentences]
32
[+] score: 4
044hsa-miR-18b2.20.014hsa-miR-423-5p1.70.048hsa-miR-932.10.014hsa-miR-1911.50.049hsa-miR-548b-5p2.30.015Downregulated miRNAs  hsa-miR-252.10.015hsa-miR-885-5p-4.20.00011hsa-miR-324-3p2.30.017hsa-miR-874-5.80.00018hsa-miR-3262.60.017hsa-miR-486-3p-4.60.00040hsa-miR-18a3.10.017hsa-miR-299-5p-4.20.0020hsa-miR-20b2.00.017hsa-miR-488-3.90.0063hsa-miR-1942.80. [score:4]
[1 to 20 of 1 sentences]
33
[+] score: 4
In this context, we observed a preferential down-regulation in region 14q32.31 including miRNA miR-127, miR-370, miR-299, miR-154, miR-154*, miR-323, miR-134, miR-368 and miR-337. [score:4]
[1 to 20 of 1 sentences]
34
[+] score: 4
Our results also confirmed other miRNAs that are upregulated in hES cells such as miR-299-3p, miR-369-3p, miR-96 and miR-372[16, 17, 24, 25]. [score:4]
[1 to 20 of 1 sentences]
35
[+] score: 4
Our results showed that the expression patterns of miR-1, miR-133a, miR-133b, miR-144, miR-206, miR-299, miR-331 and miR-4286 (Additional file 3: Figure S3) were significantly different in the three stages (p < 0.01), indicating that they may participate in the regulation of follicular transition. [score:4]
[1 to 20 of 1 sentences]
36
[+] score: 4
miR-299-5p and -335* were the 2 most highly expressed miRNAs in influenza patients (Table 1). [score:3]
miR-299-5p and miR-30a did not have any predicted interaction sites with influenza A genome. [score:1]
[1 to 20 of 2 sentences]
37
[+] score: 4
Particularly, among the down-regulated miRNAs the set of miR-124a, miR-189, miR-299-5p and miR-379, was previously reported associated with autoimmune disorders [17]. [score:4]
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38
[+] score: 3
miR-299-3p was completely identical across all primates except for a single change (C10T) in humans. [score:1]
The secondary structure of miR-299 was entirely conserved (SCI = 1) and was the most thermodynamically stable hairpin of all the miRNA in this study (z = -10.33). [score:1]
miR-299-3p. [score:1]
[1 to 20 of 3 sentences]
39
[+] score: 3
Cahill and colleagues have shown that human derived BRAFT1799A- and RET/PTC-bearing thyroid tumor cells, KAT10 and TPC-1 respectively, express lower levels of 14q32-encoded miRNAs miR-323-3p, miR-370-5p, miR-127-3p, miR-299 and miR-154 [22, 23]. [score:3]
[1 to 20 of 1 sentences]
40
[+] score: 3
miR-485-3p, together with miR-154, miR-299-5p, miR-376a, etc, is mapped to the 14q32.31 region in which allelic deletions [33] and translocations [34] are frequently identified in cancer, suggesting that miR-485-3p may be a tumor suppressor. [score:3]
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41
[+] score: 3
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-let-7c, hsa-let-7d, hsa-let-7e, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-19a, hsa-mir-20a, hsa-mir-23a, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-25, hsa-mir-26a-1, hsa-mir-30a, hsa-mir-33a, hsa-mir-96, hsa-mir-98, hsa-mir-103a-2, hsa-mir-103a-1, mmu-let-7g, mmu-let-7i, mmu-mir-23b, mmu-mir-30a, mmu-mir-30b, mmu-mir-99b, mmu-mir-125a, mmu-mir-125b-2, mmu-mir-9-2, mmu-mir-133a-1, mmu-mir-146a, mmu-mir-155, mmu-mir-182, mmu-mir-183, mmu-mir-24-1, mmu-mir-191, mmu-mir-199a-1, hsa-mir-199a-1, mmu-mir-200b, hsa-mir-30c-2, hsa-mir-30d, mmu-mir-30e, hsa-mir-181b-1, hsa-mir-182, hsa-mir-183, hsa-mir-199a-2, hsa-mir-199b, hsa-mir-221, hsa-mir-223, hsa-mir-200b, mmu-mir-299a, mmu-let-7d, hsa-let-7g, hsa-let-7i, hsa-mir-23b, hsa-mir-30b, hsa-mir-125b-1, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-191, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-125a, hsa-mir-125b-2, hsa-mir-146a, mmu-mir-30c-1, mmu-mir-30c-2, mmu-mir-30d, mmu-let-7a-1, mmu-let-7a-2, mmu-let-7b, mmu-let-7c-1, mmu-let-7c-2, mmu-let-7e, mmu-let-7f-1, mmu-let-7f-2, mmu-mir-20a, mmu-mir-21a, mmu-mir-23a, mmu-mir-24-2, mmu-mir-26a-1, mmu-mir-96, mmu-mir-98, mmu-mir-103-1, mmu-mir-103-2, mmu-mir-148b, mmu-mir-351, hsa-mir-200c, hsa-mir-155, hsa-mir-181b-2, mmu-mir-19a, mmu-mir-25, mmu-mir-200c, mmu-mir-223, mmu-mir-26a-2, mmu-mir-221, mmu-mir-199a-2, mmu-mir-199b, mmu-mir-9-1, mmu-mir-9-3, mmu-mir-181b-1, mmu-mir-125b-1, hsa-mir-30c-1, hsa-mir-99b, hsa-mir-30e, hsa-mir-26a-2, hsa-mir-361, mmu-mir-361, hsa-mir-365a, mmu-mir-365-1, hsa-mir-365b, hsa-mir-375, mmu-mir-375, hsa-mir-148b, mmu-mir-133a-2, mmu-mir-133b, hsa-mir-133b, mmu-mir-181b-2, mmu-mir-433, hsa-mir-429, mmu-mir-429, mmu-mir-365-2, hsa-mir-433, hsa-mir-490, hsa-mir-193b, hsa-mir-92b, mmu-mir-490, mmu-mir-193b, mmu-mir-92b, hsa-mir-103b-1, hsa-mir-103b-2, mmu-mir-299b, mmu-mir-133c, mmu-let-7j, mmu-mir-30f, mmu-let-7k, mmu-mir-9b-2, mmu-mir-9b-1, mmu-mir-9b-3
The 3′ UTR of mouse Xbp1 mRNA contains several putative target sites for miR-199, miR-299, miR-433, miR-221, and miR-490. [score:3]
[1 to 20 of 1 sentences]
42
[+] score: 3
On the one hand, the CARE is targeted by at least four different miRNAs (miR-297, miR-299, miR-567, and miR-609) and by the heterogeneous nuclear ribonucleoprotein L (hnRNP L). [score:3]
[1 to 20 of 1 sentences]
43
[+] score: 3
However, we identified maternally-expressed miRNAs (miR-299 and miR-654) in both offspring (Fig.   4d). [score:3]
[1 to 20 of 1 sentences]
44
[+] score: 2
Formosa A, Markert EK, Lena AM, Italiano D, Finazzi-Agro E, Levine AJ, et al. s, miR-154, miR-299-5p, miR-376a, miR-376c, miR-377, miR-381, miR-487b, miR-485-3p, miR-495 and miR-654-3p, mapped to the 14q32.31 locus, regulate proliferation, apoptosis, migration and invasion in metastatic prostate cancer cells. [score:2]
[1 to 20 of 1 sentences]
45
[+] score: 1
01720Xhsa-miR-652-3p0.1640.00214Xhsa-miR-1273 g-3p0.3820.005491hsa-miR-21-5p0.1650.0005917hsa-miR-4668-5p0.3860.000139hsa-miR-142-5p0.1750.0005617hsa-miR-20b-3p0.3900.01073Xhsa-miR-36530.1780.0011722hsa-miR-148a-3p0.3910.000757hsa-miR-27b-3p0.1880.001339hsa-miR-483-3p0.3921.4E-0511hsa-miR-299-3p0.1910.0011214hsa-miR-44500.3930.000684hsa-miR-1260a0.1937.5E-0514hsa-miR-93-5p0.4000.007367hsa-miR-4445-5p0.2028.2E-053hsa-miR-56840.4050. [score:1]
[1 to 20 of 1 sentences]
46
[+] score: 1
73(12) hsa-miR-377* 14q32.2 −2.72 hsa-miR-7 15q25.3/19p13.3/9q21.32 −2.72(12, 14) hsa-miR-124 20p23.1/8q12.3/8p23.1 −2.71(12, 14, 29, 48, 49) hsa-miR-323-5p 14q32.31 −2.69(12) hsa-miR-873 9p21.1 −2.65 hsa-miR-129* 11p11.2/7q32.1 −2.63 hsa-miR-338-5p 17q25.3 −2.61(14) hsa-miR-409-5p 14q32.2 −2.61 hsa-miR-874 5q31.2 −2.46 hsa-miR-495 14q32.2 −2.46(52) hsa-miR-885-5p 3p25.3 −2.45 hsa-miR-376c 14q32.2 −2.43(52) hsa-miR-299-5p 14q32.2 −2.41 hsa-miR-539 14q32. [score:1]
[1 to 20 of 1 sentences]
47
[+] score: 1
The set includes miR-127, miR-154, miR-154*, miR-299, miR-323, miR-368, and miR-370. [score:1]
[1 to 20 of 1 sentences]
48
[+] score: 1
Nine of those 11 miRNAs including miR-433, miR-127, miR-381, miR-377, miR-299-3p, miR-409-3p, miR-154, miR-382, and miR-376c are associated with OS. [score:1]
[1 to 20 of 1 sentences]
49
[+] score: 1
The set includes miR-127, miR-154, miR-154*, miR-299, miR-323, miR-368, and miR-370. [score:1]
[1 to 20 of 1 sentences]
50
[+] score: 1
PCA plot reveals the distinct sample clusters for metastatic tumours and non-metastatic tumours The following ten microRNAs were selected for validation of microarray results: cfa-let-7c, cfa-miR-10b, cfa-miR-26a, cfa-miR-26b, cfa-miR-29c, cfa-miR-30a, cfa-miR-30b, cfa-miR-30c, cfa-miR-148a and cfa-miR-299. [score:1]
[1 to 20 of 1 sentences]
51
[+] score: 1
Other miRNAs from this paper: hsa-let-7f-1, hsa-let-7f-2, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-25, hsa-mir-32, mmu-mir-1a-1, mmu-mir-133a-1, mmu-mir-134, mmu-mir-135a-1, mmu-mir-144, mmu-mir-181a-2, mmu-mir-24-1, mmu-mir-200b, mmu-mir-206, hsa-mir-208a, mmu-mir-122, hsa-mir-181a-2, hsa-mir-181b-1, hsa-mir-181c, hsa-mir-181a-1, hsa-mir-214, hsa-mir-200b, mmu-mir-299a, mmu-mir-302a, hsa-mir-1-2, hsa-mir-122, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-135a-1, hsa-mir-135a-2, hsa-mir-144, hsa-mir-134, hsa-mir-206, mmu-mir-200a, mmu-mir-208a, mmu-let-7f-1, mmu-let-7f-2, mmu-mir-24-2, mmu-mir-328, hsa-mir-200c, hsa-mir-1-1, mmu-mir-1a-2, hsa-mir-181b-2, mmu-mir-25, mmu-mir-32, mmu-mir-200c, mmu-mir-181a-1, mmu-mir-214, mmu-mir-135a-2, mmu-mir-181b-1, mmu-mir-181c, hsa-mir-200a, hsa-mir-302a, hsa-mir-361, mmu-mir-361, hsa-mir-302b, hsa-mir-302c, hsa-mir-302d, hsa-mir-367, hsa-mir-377, mmu-mir-377, hsa-mir-328, mmu-mir-133a-2, mmu-mir-133b, hsa-mir-133b, mmu-mir-181b-2, hsa-mir-20b, hsa-mir-429, mmu-mir-429, hsa-mir-483, hsa-mir-486-1, hsa-mir-181d, mmu-mir-483, mmu-mir-486a, mmu-mir-367, mmu-mir-20b, hsa-mir-568, hsa-mir-656, mmu-mir-302b, mmu-mir-302c, mmu-mir-302d, mmu-mir-744, mmu-mir-181d, mmu-mir-568, hsa-mir-892a, hsa-mir-892b, mmu-mir-208b, hsa-mir-744, hsa-mir-208b, mmu-mir-1b, hsa-mir-302e, hsa-mir-302f, hsa-mir-1307, eca-mir-208a, eca-mir-208b, eca-mir-200a, eca-mir-200b, eca-mir-302a, eca-mir-302b, eca-mir-302c, eca-mir-302d, eca-mir-367, eca-mir-429, eca-mir-328, eca-mir-214, eca-mir-200c, eca-mir-24-1, eca-mir-1-1, eca-mir-122, eca-mir-133a, eca-mir-144, eca-mir-25, eca-mir-135a, eca-mir-568, eca-mir-133b, eca-mir-206-2, eca-mir-1-2, eca-let-7f, eca-mir-24-2, eca-mir-134, eca-mir-299, eca-mir-377, eca-mir-656, eca-mir-181a, eca-mir-181b, eca-mir-32, eca-mir-486, eca-mir-181a-2, eca-mir-20b, eca-mir-361, mmu-mir-486b, mmu-mir-299b, hsa-mir-892c, hsa-mir-486-2, eca-mir-9021, eca-mir-1307, eca-mir-744, eca-mir-483, eca-mir-1379, eca-mir-7177b, eca-mir-8908j
On contrary, four of liver-specific miRNAs reported here were reported in Kim et al. [9] as muscle (eca-miR-299, eca-miR-32, eca-miR-656) or colon-specific miRNAs (eca-miR-429). [score:1]
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The results revealed potentially conserved sites for approximately nine miRNA family candidates (miR-30c, miR-34a/c, miR-449b, miR-181, miR-301a, miR-421, miR-299-5p, miR-609 and miR-99a) in the PAI-1 mRNA 3′ UTR. [score:1]
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We also analyzed the “pluripotent” miRNAs identified previously [26, 27] in human iPSCs and hESCs, specifically miR-302, miR-367–371, mi-17–92, miR-299, and mi-Let 7 cluster, and found high correlation between the WA09 human embryonic stem cell (hESC) line and the iPSC line generated with Sendai virus vector (R [2] = 0.9662). [score:1]
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Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-let-7c, hsa-let-7d, hsa-let-7e, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-16-1, hsa-mir-17, hsa-mir-21, hsa-mir-23a, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-25, hsa-mir-26a-1, hsa-mir-26b, hsa-mir-30a, hsa-mir-31, hsa-mir-96, hsa-mir-99a, hsa-mir-16-2, hsa-mir-30c-2, hsa-mir-30d, hsa-mir-182, hsa-mir-183, hsa-mir-211, hsa-mir-217, hsa-mir-218-1, hsa-mir-218-2, hsa-mir-221, hsa-mir-222, hsa-let-7g, hsa-let-7i, hsa-mir-15b, hsa-mir-23b, hsa-mir-30b, hsa-mir-125b-1, hsa-mir-132, hsa-mir-143, hsa-mir-145, hsa-mir-191, hsa-mir-125a, hsa-mir-125b-2, hsa-mir-126, hsa-mir-184, hsa-mir-190a, hsa-mir-195, rno-mir-322-1, rno-let-7d, rno-mir-335, rno-mir-342, rno-mir-135b, hsa-mir-30c-1, hsa-mir-30e, hsa-mir-26a-2, hsa-mir-379, hsa-mir-382, hsa-mir-342, hsa-mir-135b, hsa-mir-335, rno-let-7a-1, rno-let-7a-2, rno-let-7b, rno-let-7c-1, rno-let-7c-2, rno-let-7e, rno-let-7f-1, rno-let-7f-2, rno-let-7i, rno-mir-15b, rno-mir-16, rno-mir-17-1, rno-mir-21, rno-mir-23a, rno-mir-23b, rno-mir-24-1, rno-mir-24-2, rno-mir-25, rno-mir-26a, rno-mir-26b, rno-mir-30c-1, rno-mir-30e, rno-mir-30b, rno-mir-30d, rno-mir-30a, rno-mir-30c-2, rno-mir-31a, rno-mir-96, rno-mir-99a, rno-mir-125a, rno-mir-125b-1, rno-mir-125b-2, rno-mir-126a, rno-mir-132, rno-mir-143, rno-mir-145, rno-mir-183, rno-mir-184, rno-mir-190a-1, rno-mir-191a, rno-mir-195, rno-mir-211, rno-mir-217, rno-mir-218a-2, rno-mir-218a-1, rno-mir-221, rno-mir-222, rno-mir-299a, hsa-mir-384, hsa-mir-20b, hsa-mir-409, hsa-mir-412, hsa-mir-489, hsa-mir-494, rno-mir-489, rno-mir-412, rno-mir-543, rno-mir-542-1, rno-mir-379, rno-mir-494, rno-mir-382, rno-mir-409a, rno-mir-20b, hsa-mir-542, hsa-mir-770, hsa-mir-190b, hsa-mir-543, rno-mir-466c, rno-mir-17-2, rno-mir-182, rno-mir-190b, rno-mir-384, rno-mir-673, rno-mir-674, rno-mir-770, rno-mir-31b, rno-mir-191b, rno-mir-299b, rno-mir-218b, rno-mir-126b, rno-mir-409b, rno-let-7g, rno-mir-190a-2, rno-mir-322-2, rno-mir-542-2, rno-mir-542-3
Similarly, stepwise artificial neural networks analysis revealed predictive miRNA signatures (miR-342, miR-299, miR-217, miR-190, miR-135b, miR-218) corresponding to oestrogen receptor status in breast cancer [39]. [score:1]
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Similarly, elevation of miR-299-3p (MIMAT0000687), as observed in the HEa group, has been shown to result in senescence of umbilical vein endothelial cells [57] which may also impair fetal growth. [score:1]
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