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19 publications mentioning hsa-mir-659

Open access articles that are associated with the species Homo sapiens and mention the gene name mir-659. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

1
[+] score: 217
Figure 2(A) Expression of miR-659-3p, (B) miR-572, (C) CNOT1, GSTE1 and KIF4A and (D) inverse correlation between miR-659-3p and CNOT1 expression in HTLA-230 and SH-SY5Y cells treated with miR-659-3p mimic and inhibitorResults of RT-qPCR analysis from two independent experiments are reported as Log [10] of relative expression respect to that occurring in cells treated with irrelevant miRNA mimic and inhibitor. [score:11]
Studies in NB cell lines treated with miR-659-3p mimic and inhibitor indicated that miR-659-3p specifically modifies the expression of the transcription factor CNOT1, and the expression of the AU-rich element (ARE)-containing target genes AKT3, BCL2, CYR61 and THSB2, that belong to the focal adhesion pathway. [score:9]
To identify miR-659-3p target genes, the whole genome expression profiles of HTLA-230 and SH-SY5Y cells transfected with miR-659-3p mimic and inhibitor were compared to those of cells transfected with irrelevant miRNA mimic and inhibitor, respectively. [score:8]
As shown in Figure 2A, treatment with miR-659-3p mimic and inhibitor respectively increased and decreased miR-659-3p expression as compared to cells treated with the irrelevant mimic and inhibitor, whereas the expression of the unrelated miR-572 was unaffected (Figure 2B). [score:8]
Thirty-four genes more expressed in BM-infiltrating cells than primary tumors were also more expressed in the NB cell lines treated with the miR-659-3p inhibitor (Table 3). [score:7]
Moreover, in NB cell lines treated with miR-659-3p mimic and inhibitor, CNOT1 expression levels inversely correlated to miR-659-3p expression levels (Figure 2D). [score:7]
Effects of miR-659-3p over -expression and suppression on gene expression. [score:7]
Microarray data were analyzed as described in the statistical analysis section, and the probes whose expression was specifically modified by the miR-659-3p mimic and inhibitor were merged to the probes differentially expressed by BM-infiltrating cells and primary tumors ([10], GEO accession number GSE 25623a). [score:7]
Since miR-516a-3p was expressed at the same level in the normal adrenal gland and NB cell lines, whereas miR-659-3p was not expressed by the adrenal gland and highly expressed in NB cell lines, we selected this latter miRNA for further studies. [score:7]
Since CNOT1 encodes a transcription factor that degrades mRNAs containing ARE sequences [28], over -expression of CNOT1, subsequent to decreased expression of miR-659-3p, should reduce the expression of ARE-containing genes. [score:7]
Results are shown as Log [10] relative expression with respect to that of cells transfected with the irrelevant mimic and inhibitor set to 1. Total RNA extracted from HTLA-230 and SH-SY5Y cells transfected with miR-659-3p and irrelevant mimic and inhibitor from the two experiments were pooled. [score:7]
The higher expression of CNOT1 driven by the lower expression of miR-659-3p leaded to reduced expression of four ARE-containing mRNAs, AKT3, BCL2, CYR61 and THBS2, belonging to the focal adhesion pathway. [score:7]
Six miRNAs, 3 less expressed (miR-324-3p, miR-516a-3p, miR-659-3p) and 3 more expressed (miR-137, miR-301a-3p, miR-873-5p) in BM-infiltrating cells than in primary tumors, were significantly differentially expressed also in this new set of samples (Table 2). [score:7]
To evaluate the effect of miR-659-3p over -expression and suppression on gene expression, 1×10 [6] HTLA-230 and SH-SY5Y cells were transfected with specific miR-659-3p mirVana™ mimic and inhibitor, respectively (Ambion, Life Technologies, Carlsbad, CA, USA, catalog# MC and MH 11582). [score:7]
As shown in Figure 2C, RT-qPCR analysis confirmed that CNOT1 expression was specifically and significantly modified by miR-659-3p mimic and inhibitor treatment, whereas GTSE1 and KIF4A expression was not affected by the treatment. [score:7]
In the miR-659-3p -transfected NB cell lines, the expression of AKT3, BCL2, CYR61 and THSB2 was confirmed to be specifically modified by miR-659-3p mimic and inhibitor, whereas that of RNASEL was not affected by the treatment and that of HEY1 and ZNF652 occurred in the wrong direction (Figure 3). [score:6]
Thus, ten BM-infiltrating cells and ten primary tumors were analyzed by RT-qPCR to confirm that miR-659-3p reduced expression in BM-infiltrating cells associated to over -expression of CNOT1 and reduced expression of AKT3, BCL2, CYR61 and THBS2 genes, as compared to primary tumors. [score:6]
of the eight profiles demonstrated that the expression of 2073 probes was specifically and inversely modified by miR-659-3p mimic and inhibitor (Supplementary Data). [score:5]
b Genes up-modulated following miR-659-3p over -expression, down-modulated following miR-659-3p suppression, down-modulated in BM-infiltrating cells. [score:5]
Expression levels of genes containing ARE-sequence in HTLA-230 and SH-SY5Y cells treated with miR-659-3p mimic and inhibitor. [score:5]
Differential whole gene expression analysis of cell lines transfected with miR-659-3p and irrelevant mimic and inhibitor was performed using the limma package of Bioconductor [42, 43]. [score:5]
Taken together the results of our study support the hypothesis that the metastatic process in human NB involves alteration of the focal adhesion pathway, through the increased expression of CNOT1, driven by decreased expression of miR-659-3p. [score:5]
We thus checked the 51 genes differentially expressed by BM-infiltrating cells and primary tumors, and over-expressed in NB cell lines treated with miR-659-3p mimic (Table 3), for the presence of ARE sequence by consulting the http://brp. [score:5]
In vitro experiments with miR-659-3p mimic and inhibitor allowed to identify CNOT1 as its target gene in human NB. [score:5]
This finding supports the hypothesis that the metastatic process in human NB involves alteration of the focal adhesion pathway by regulation of CNOT1 levels determined in turn by miR-659-3p expression level. [score:4]
Indeed, in BM-infiltrating cells, the lower expression of miR-659-3p associated to higher levels of CNOT1 and lower expression of AKT3, BCL2, CYR61 and THBS2 mRNAs, as compared to primary tumors. [score:4]
Adjuvant therapy with AKT activators or metallo-protease inhibitors, together with targeted delivery of miR-659-3p mimic, could be considered in relapsed or refractory stage M NB patients. [score:4]
These genes were checked for the presence of 3′-UTR sequence recognized by miR-659-3p by TargetScan (www. [score:3]
Several miRNAs other than miR-659-3p differentially expressed by NB tumors and metastases may deserve further attention as potential drivers of the metastatic process. [score:3]
To evaluate the role of miR-659-3p and its target genes in the metastatic process, the HTLA-230 and SH-SY5Y NB cell lines were transfected with specific miR-659-3p or irrelevant miRNA mimic and inhibitor. [score:3]
Thus, avoiding the disruption of the structural architecture by increasing miR-659-3p expression may dampen the metastatic process. [score:3]
The differential expression of these genes was already reported by us [10], but their relationships were unknown, as well as with miR-659-3p. [score:3]
In addition, miR-659-3p was not expressed in normal adrenal gland, supporting its role in the neoplastic process. [score:3]
Indeed, BM-infiltrating cells express lower level of miR-659-3p, higher level of CNOT1 and lower levels of AKT3, BCL2, THSB2 and CYR61 than NB primary tumors. [score:3]
To confirm increase and decrease of miR-659-3p expression following transfection with miR- mimic and inhibitor, respectively, the miRNA fraction isolated from each transfected cells was reverse transcribed using the Megaplex RT Primers Human Pool A and B and then amplified with the TaqMan [©] human miR-659-3p assay in triplicates in a 96 well plate. [score:3]
After screening the significant miRNAs for level and distribution of expression values in the two groups of samples, we focused on miR-659-3p. [score:3]
In all sets of samples from stage M NB patients, miR-659-3p expression resulted significantly lower in BM-infiltrating cells than in primary tumors. [score:3]
Taken together, these findings demonstrated that CNOT1 expression in NB cells was specifically modified by miR-659-3p. [score:3]
Of these three miRNAs, miR-516a-3p and miR-659-3p were significantly less expressed in BM-infiltrating cells than in primary tumors in all sets of samples (Table 2). [score:3]
Genes specifically modulated by treatment with miR-659-3p mimic, known to be differentially expressed by BM-infiltrating cells and primary tumors. [score:3]
Here, the analysis of ten additional BM-infiltrating and primary tumors and four paired BM-infiltrating cells and corresponding primary tumors demonstrated that miR-659-3p was always less expressed in human NB metastases as compared to primary tumors. [score:2]
To validate the differential expression of the selected 20 miRNAs, reverse-transcribed and pre-amplified miRNA fractions from 10 additional BM-infiltrating and 10 primary tumors were amplified in a 96 well plate in triplicate using the specific TaqMan [©] human microRNA assays (hsa-miR-324-3p, catalog #002161; hsa-miR-516-3p, catalog #001149; hsa-miR-628-5p, catalog #002433; hsa-miR-659-3p, catalog #001514; hsa-miR-10b, catalog #002218; hsa-miR-128, catalog #002216; mmu-miR-137, catalog #01129; mmu-miR-140, catalog #001187; hsa-miR-16, catalog #000391, hsa-miR-191, catalog #002299; hsa-miR-301, catalog #000528; hsa-miR-361-3p, catalog #002116; hsa-miR-365, catalog #001020; hsa-miR-548d-3p, catalog #001605; hsa-miR-572, catalog #001614; hsa-miR-576-5p, catalog #002350, hsa-miR-616, catalog #001589; hsa-miR-628-3p, catalog #002434; hsa-miR-873, catalog #002356; hsa-miR-98, catalog #000577; U6 snRNA, catalog #001973, Life Technologies). [score:2]
To evaluate gene expression levels in miR-659-3p transfected cells, 150 ng of total RNA was reverse transcribed as described [8, 38], and then amplified in triplicate with the specific TaqMan [©] human gene expression assay (CNOT1: Hs00406740_m1, GTSE1: Hs00212681_m1, KIF4A: Hs00602211_g1, AKT3: Hs00987350_m1, BCL2: Hs00608023_m1, CYR61: Hs00998500_g1, HEY1: Hs01114113_m1, RNASEL: Hs00221692_m1, THBS2: Hs01568063_m1, ZNF652: Hs00977533_m1), and for HPRT1 (Hs99999909_m1) as endogenous reference gene (Life Technologies). [score:2]
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2
[+] score: 78
We have utilized a novel integrative analysis of miRNA and gene expression data to identify molecular biomarkers of PFS and response and found miR-659-3p expression to be positively associated with longer PFS, distinguishing patients with disease that is responsive to CP -based therapy. [score:7]
High miR-659-3p expression distinguished patients with responsive disease (complete or partial response) from patients with stable disease. [score:7]
miR-659-3p predicted gene targets include NFIX, which is a transcription factor known to interact with c-Jun and AP-1 in the context of developmental processes and disease. [score:6]
However, the expression of most of those genes was not significantly anti-correlated with miR-659-3p expression. [score:5]
miR-659-3p was not differentially expressed based on the treatment arm (CP with sorafenib vs CP without sorafenib; p = 0.6), BRAF mutation status (mutant vs wild-type; p = 0.34) or NRAS mutation status (mutant vs wild-type; p = 0.55). [score:5]
While the association between miR-659-3p and these predicted genes targets is intriguing, it is important to note that our gene expression data do not show strong correlations with miR-659-3p and at this point, these findings are not confirmed. [score:5]
Of particular significance in our study is the identification of gene targets predicted for miR-659-3p and the construction of a proposed regulatory network which may lend insight into the mechanistic role of miR-659-3p in response to cytotoxic chemotherapy in melanoma. [score:4]
However, we did find a significant anti-correlation (p < 0.01) between miR-659-3p and its predicted targets COG6, ENOX2, HCFC2, NFIX, SDC1, and TSC22D2 (Fig.   2a). [score:3]
Dichotomized by median PFS (less vs greater than 4 months), miR-659-3p expression was significantly different. [score:3]
miR-659-3p gene targets. [score:3]
We also noticed that higher miR-659-3p expression was generally observed in patients who achieved an objective response (complete or partial response) as opposed to patients with stable disease by Response Evaluation Criteria In Solid Tumors (RECIST) (p = 0.04. ) [score:3]
Target predictions of miR-659-3p identified utilizing mirConnX software for network inference (b). [score:3]
Predicted gene targets of miR-659-3p selected in our analysis are genes important to the MAP kinase signaling pathway, in particular BRAF and NRAS, and genes relevant to the PI3K/MTOR, FGFR, and RAC1 pathways, as well as genes involved in DNA repair. [score:3]
Higher miR-659-3p expression remained prognostic of longer PFS (p = 0.03). [score:3]
Characterization of the functional significance of miR-659-3p has been limited to the neuroscience literature, where it has been shown to bind a common genetic variant of and regulate the expression of the gene progranulin, which may significantly increase the risk for frontotemporal dementia [35]. [score:2]
The value of the proposed regulatory network is to inform upon pathways which should be interrogated as we continue to elucidate the role of miR-659-3p as a predictive biomarker. [score:2]
While our proposed regulatory network embeds miR-659-3p in the landscape of melanoma signaling, functional studies are paramount to the validation of this miRNA as a mediator of melanoma signaling. [score:2]
The miR-659-3p cluster also included miR-219-3p and miR-519-5p (Fig.   1b), which had less significant or no association with PFS (p = 0.036 and p = 0.12, respectively). [score:1]
Independent validation of the predictive value of miR-659-3p is currently ongoing in an independent cohort of MM patients treated with carboplatin and paclitaxel. [score:1]
Rademakers R Eriksen JL Baker M Robinson T Ahmed Z Lincoln SJ Common variation in the miR-659 binding-site of GRN is a major risk factor for TDP43 -positive frontotemporal dementiaHum Mol Genet. [score:1]
This novel integrative analysis suggests miR-659-3p as a candidate biomarker of response in MM patients treated with platinum -based chemotherapy and may serve to improve patient selection. [score:1]
The functional significance of miR-659-3p in cancer and melanoma is as of yet unknown. [score:1]
Patients are ordered from shortest to longest progression-free survival (c) T-ReCS identified miR-659-3p as the primary miRNA associated positively with PFS (p = 0.008). [score:1]
We did find a significant anti-correlation between miR-659-3p and a small set of genes. [score:1]
This interaction may represent a clue as to functional relevance of miR-659-3p and requires further validation. [score:1]
miR-659-3p is associated with improved PFS in metastatic melanoma. [score:1]
Our study identified an association between miR-659-3p and the clinical activity of CP -based therapy implicating miR-659-3p as a candidate predictive biomarker in patients with metastatic melanoma. [score:1]
This novel integrative analysis implicates miR-659-3p as a candidate predictive biomarker for MM patients treated with platinum -based chemotherapy and may serve to improve patient selection. [score:1]
T-ReCS identified PLXNB1 as negatively associated with progression-free survival (PFS) and miR-659-3p as the primary miRNA associated positively with PFS. [score:1]
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3
[+] score: 22
The pathway of PGRN or PGRN itself is influenced by several miRNA including miRNA-132, miRNA-659-3p, miRNA-107 and miRNA-9. The majority of miRNA with links to various diseases, as e. g., miRNA-132, have been found through profiling miRNA that are either up- or down-regulated after certain traumatic events (status epilepticus, traumatic brain injury) or in certain neurodegenerative disorders such as FTD and Alzheimer’s Disease (AD). [score:8]
Further tests showed that an increase of miRNA-659-3p caused a decreased expression of GRN -RNA, this suggests that binding of miRNA-659-3p with the GRN -RNA inhibits its translation. [score:7]
3.2. miRNA-659-3p. [score:1]
Piscopo P. Grasso M. Fontana F. Crestini A. Puopolo M. del Vescovo V. Venerosi A. Calamandrei G. Vencken S. F. Greene C. M. Reduced miR-659-3p levels correlate with progranulin increase in hypoxic conditions: Implications for frontotemporal dementia Front. [score:1]
It has also shown that miR-659-3p decreases under hypoxic conditions while the concentration of PGRN increases with a delay, probably similar to the PGRN levels seen in humans and rats. [score:1]
Therefore, it is tempting to speculate that markers of hypoxic conditions such as Hypoxia-inducible-Factor1 or miRNA-659-3p may also participate in the pathomechanisms involved during and after status epilepticus but more studies are needed to prove this. [score:1]
Since the majority of miRNA control genes through modification at the 3′UTR-end, Piscobo et al. [22] analyzed the 3′UTR-end of the GRN-gene and found two possible binding sites for miR-659-3p. [score:1]
Profiling miRNA in the human cerebral cortex has shown a far higher level of miRNA-107 than, e. g., miRNA-659-3p. [score:1]
Corresponding to the mechanism for miR-659-3p, the correlation between decreased levels of miRNA-107 and higher levels of PGRN in the affected cells indicates a neuroprotective mechanism. [score:1]
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4
[+] score: 19
PPARGC1α is a predicted target of miR-150, while IRS2 and CPT1α are predicted targets of miR-659 according to TargetScan [44]. [score:7]
Also in subcutaneous adipose tissue from obese subjects miR-150 was reported to be upregulated and miR-659 was reported to be downregulated [9]. [score:7]
Unfortunately, miR-150 and miR-659 target protein levels were found to be unchanged in obese adipose tissue [9], although this finding does not rule out the possibility miR-150 and miR-659 may act on alternative targets which remain to be identified. [score:5]
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5
[+] score: 13
Some of these genes were differentially expressed in the response to LH binding to LHR+ cancer cells, including those involved in the regulation of cell migration and proliferation (such as IRS1, IRS2, IL6R, TPM1, GLI1, BMPR2 and GRN), cell surface receptor-linked signal transduction (SOCS5 and RAF1), anti-apoptosis (FAS, MCL1 and SGK3) and transcription regulation (DNMT3B, GLI1 and EZH2), as shown in Table 1. Six genes exhibited highly correlated expression to their microRNAs (| rho|> = 0.7), including IRS1, IRS2 and RAF1 to miR-7-1, SGK3 and MTAP to miR-21 and GRN to miR-659. [score:7]
It is indicated from the expression changes that LH may impose a moderate positive regulation of cell proliferation, nucleotide metabolic process and cell surface receptor-linked signal transduction, and a negative regulation of apoptosis on ovarian cancer cells, in terms of the gene regulation through miR-7-1, miR-21 and miR-659. [score:6]
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6
[+] score: 11
We should underline that some of these miRNAs (Table 3) are expressed in the 90% of the ES patients, such as the up-regulated miR-210 (11p15.5), Let-7a (9q22.32), Let-7e (19q13.41), miR-181b (1q32.1) and the down-regulated miR-1908 (11), miR-659 (22q13.1) and miR-937 (8q24.3). [score:9]
Rademakers R. Eriksen J. L. Baker M. Robinson T. Ahmed Z. Lincoln S. J. Finch N. Rutherford N. J. Crook R. J. Josephs K. A. Common variation in the miR-659 binding-site of GRN is a major risk factor for TDP43 -positive frontotemporal dementia Hum. [score:1]
There are no reports regarding miR-659 and its association with cancer, while it was shown to be correlated with neurodegenerative disorders [42]. [score:1]
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7
[+] score: 11
We observed differing expression of miR-224 and miR-383, whereas expression of the five other candidate miRNAs: miR-610, miR-637, miR-659, miR-1202 and miR-1266 did not differ significantly between ccRCC and control tissue (Figure S1, Supplemental Data). [score:5]
Expression of miR-224, miR-383, miR-610, miR-637, miR-659, miR-1202 and miR-1266 was analyzed in 32 matched pairs of tumor (T) and control (C) samples. [score:3]
We identified 7 potential miRNAs targeting the 3′UTR of human DIO1 (Table 1): miR-224, miR-383, miR-610, miR-659, miR-637, miR-1202 and miR-1266. [score:3]
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8
[+] score: 11
0045863.g002 Figure 2 H1F0 rs1894644 × hsa-mir-659 rs5750504 interaction on H1F0 monocyte expression. [score:3]
H1F0 rs1894644 × hsa-mir-659 rs5750504 interaction on H1F0 monocyte expression. [score:3]
The second replicated interaction involved the H1F0 rs1894644 and hsa-mir-659 rs5750504 tagged by the rs763137/rs2899293 and rs1894644/rs6000905 pairs in GHS and CTS, respectively (Figure 2). [score:1]
Interestingly, hsa-mir-659 has been shown to influence the risk of dementia [46] through a mechanism that could involve histone deacetylation [47], [48]. [score:1]
Although speculative, the joint contribution of H1F0 and hsa-mir-659 on the risk of dementia could deserve further attention. [score:1]
Two interactions miSNPs × 3utrSNPs were robustly identified, the first involving HLA-DPB1 rs1042448 and hsa-mir-219-1 rs107822, the second the H1F0 rs1894644 and hsa-mir-659 rs5750504. [score:1]
Nevertheless, one cannot exclude the possibility that the detected interactions are tagging for other complex haplotypic effects spanning a large distance and over several genes, five genes lying between HLA-DPB1 and hsa-mir-219-1 and three between H1F0 and hsa-mir-659 (Figure 3). [score:1]
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9
[+] score: 10
Of these, 14 (miR-23b, miR-28, miR-98, miR-103, miR-107, miR-193a,0, miR-324-5p, miR-324-3p, miR-331, miR-374, miR-432, miR-502, and miR-660) were upregulated and 6 (miR-31, miR-451, miR-452, miR-565, miR-594 and miR-659) were downregulated. [score:7]
[27]-  57 miR-565 (n)↓(this study)-  58 miR-594 (n)↓(this study)   59 miR-659 (n)↓↓↓(this study)-   60 miR-660 (n) ↑↑↑ (this study) -    In bold are human-specific MR-miRs (hMR-miRs, 16 in total); Italicized are microRNAs shown to be differentially expressed during myogenesis in non- human cells; microRNAs with a known function in myogenesis are underscored. [score:3]
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10
[+] score: 10
Indeed, miR-659 also inhibits hPGRN expression [39]. [score:5]
Interestingly, a common genetic variant (rs5848) in the binding site of miR-659 increases the inhibition of hPGRN expression by miR-659 [39]. [score:5]
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11
[+] score: 7
MiR-510 and miR-659 were over-expressed under diabetic-like conditions and decreased after calcitriol was added. [score:3]
miR-659 and miR-411 were validated because in the microarray analysis they were significantly changed after the addition of calcitriol. [score:1]
MiR-181c, miR-15a, miR-20b, miR-411, miR-659, miR-126 and miR-510 were selected for further analysis because they are known to be modified in DM and in other biological disorders. [score:1]
MiR-659 is not described in the database as being connected to a diabetic-like environment and appears to be novel in genomic control in the presence of diabetic-like conditions affected by vitamin D. Further investigation of the effect of the miRNA on their predicted target genes is warranted. [score:1]
In addition, 10 [-10] mol/l calcitriol was given to the cells 1 h after stimulation for an additional 23 h. The miRNA set that included (A) miR-659, (B) miR-510, (C) miR-181C, (D) miR-411, (E) miR-126, (F) miR-15a, and (G) miR-20b was validated using real time PCR. [score:1]
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12
[+] score: 7
Furthermore, we found 8 miRNAs (miR-95, miR-139, miR-379, miR-429, miR-509, miR-518e, miR-542-5p, and miR-659) downregulated in both 6 h aDCs and tDCs with respect to iDCs. [score:4]
Interestingly, 5 miRNAs (miR-95, miR-429, miR-509, miR-542, and miR-659) were downregulated in tDCs and aDCs compared with iDCs. [score:3]
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13
[+] score: 6
To confirm the comparability of TLDA -based genome-wide profiling with individual quantifications, we randomly chose 10 patients and 10 controls from the learning set and further quantified these subjects' expression levels of five miRNAs (has-miR 34a, miR-432, miR-548d, miR-659 and miR-185) using quantitative RT-PCR. [score:3]
Figure S3The relations in the five miRNAs (has-miR 34a, miR-432, miR-548d, miR-659 and miR-185) expression levels between two platforms of miRNA quantification, the array -based TLDA vs. [score:3]
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14
[+] score: 6
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-21, hsa-mir-22, hsa-mir-23a, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-25, hsa-mir-26b, hsa-mir-27a, hsa-mir-31, hsa-mir-33a, hsa-mir-99a, hsa-mir-100, hsa-mir-29b-1, hsa-mir-29b-2, hsa-mir-103a-2, hsa-mir-103a-1, hsa-mir-199a-1, hsa-mir-148a, hsa-mir-147a, hsa-mir-34a, hsa-mir-182, hsa-mir-199a-2, hsa-mir-212, hsa-mir-221, hsa-mir-224, hsa-let-7g, hsa-let-7i, hsa-mir-27b, hsa-mir-30b, hsa-mir-125b-1, hsa-mir-130a, hsa-mir-132, hsa-mir-142, hsa-mir-145, hsa-mir-152, hsa-mir-153-1, hsa-mir-153-2, hsa-mir-125a, hsa-mir-125b-2, hsa-mir-127, hsa-mir-134, hsa-mir-200c, hsa-mir-106b, hsa-mir-361, hsa-mir-148b, hsa-mir-20b, hsa-mir-410, hsa-mir-202, hsa-mir-503, hsa-mir-33b, hsa-mir-643, bta-let-7f-2, bta-mir-103-1, bta-mir-148a, bta-mir-21, bta-mir-221, bta-mir-26b, bta-mir-27a, bta-mir-99a, bta-mir-125a, bta-mir-125b-1, bta-mir-145, bta-mir-199a-1, bta-mir-27b, bta-mir-30b, bta-mir-31, bta-mir-127, bta-mir-142, bta-mir-20b, bta-let-7d, bta-mir-132, bta-mir-148b, bta-mir-200c, bta-mir-22, bta-mir-23a, bta-mir-29b-2, bta-mir-361, bta-let-7g, bta-mir-24-2, bta-let-7a-1, bta-let-7f-1, bta-let-7i, bta-mir-25, bta-let-7a-2, bta-let-7a-3, bta-let-7b, bta-let-7c, bta-let-7e, bta-mir-103-2, bta-mir-125b-2, bta-mir-34a, hsa-mir-708, hsa-mir-147b, hsa-mir-877, hsa-mir-940, hsa-mir-548j, hsa-mir-302e, hsa-mir-103b-1, hsa-mir-103b-2, bta-mir-100, bta-mir-106b, bta-mir-130a, bta-mir-134, bta-mir-147, bta-mir-152, bta-mir-153-1, bta-mir-153-2, bta-mir-182, bta-mir-24-1, bta-mir-199a-2, bta-mir-202, bta-mir-212, bta-mir-224, bta-mir-33a, bta-mir-33b, bta-mir-410, bta-mir-708, bta-mir-877, bta-mir-940, bta-mir-29b-1, bta-mir-148c, bta-mir-503, bta-mir-148d
Unst) Pathways in cancer miR-659, −141, −190, −449a, −200c, −361-5p, −145 9.51E-12 KRAS, PTEN, VEGFA, STAT5B, MITF, BCL2 MAPK signaling pathway miR-23a, −23b, −141, −145, −200c, −92a, −125b, −24 2.94E-11 MKNK2, MEF2C, FGF, SOS1, RAS, MAerkPK2 Wnt signaling pathway miR-125b, −449a, −302e, −145, −23a, −29b-2-5p, −659, −200c 2.76E-08 LRP5, LRP6, TCF7, PLCB4, DVL3, WNT1, WNT5A ErbB signaling pathway miR-23a, −23b, −125b, −206, −302e, −513c 3.19E-07 ERBB4, GRB2, SHC1, PIK3R3, PIK3CD, AKT3 Colorectal cancer miR-659, 23a, −23b, −141, −190, −449a, −200c, −361-5p, −145 4.48E-07 DCC, APPL1, TGFBR2, SMAD3, SMAD4, APC Axon guidance miR-23a, −23b, −200c, −145 7.23E-07 PLXNC1, EFNB2, PAK4, DCC, SEMA6A, PAK7, MET Neurotrophin signaling pathway miR-302e, −361-5p, −452, −525-5p, −449a, −659 1.82E-06 NTRK2, NGFR, KRAS, MAP3K1, PIK3R3, PLCG1 Renal cell carcinoma miR-659, −141, −190, −449a, −200c, −361-5p, −145 3.75E-05 GAB1, MET, SOS1, GRB2, VEGFA, NRAS Focal adhesion miR-24, −27b, −125a-3p, −139-5p, −206, −200c 5.04E-05 ITGB3, PXN, SHC3, ACTB, SRC, PAK2 Regulation of actin cytoskeleton miR-200c, −145, −27b, −92a, −300, −206 8.29E-05 RAC1, ROCK2, GIT1, PIK3R3, ITGA3, LIMK1 Table 3List of enriched pathways (P < 0.05), in which genes predicted to be targeted by differentially expressed miRNAs (P < 0.05) in blood plasma of hyperstimulated vs. [score:6]
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[+] score: 5
miR-659 had been shown to target a growth factor, progranulin (GRN; [30]), and the increased expression thereof may indicate the repression of GRN. [score:5]
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[+] score: 4
The expression of 4 miRNA (3 down-regulated: hsa-miR-30a, hsa-miR-29a and hsa-miR-125b and one non-regulated: hsa-miR-659) was investigated in the 6 cell lines, compared to a pool of non -treated primary cultures (Figure S2). [score:4]
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[+] score: 4
The rs5848 SNP, associated with TDP43 -positive frontotemporal dementias, is located in the miR-659 target site of the Progranulin gene, also affecting the miRNA -mediated repression (Rademakers et al., 2008). [score:3]
Common variation in the miR-659 binding-site of GRN is a major risk factor for TDP43 -positive frontotemporal dementia. [score:1]
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[+] score: 1
According to miRBase annotation, hsa-mir-1277, hsa-mir-376a-2, hsa-mir-495, hsa-mir-659, hsa-mir-1303, hsa-mir-1307 and so on encode mature miRNA at only their 3p arms. [score:1]
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[+] score: 1
Other miRNAs from this paper: hsa-mir-25, hsa-mir-28, hsa-mir-95, mmu-mir-151, mmu-mir-290a, mmu-mir-297a-1, mmu-mir-297a-2, mmu-mir-130b, mmu-mir-340, mmu-mir-25, mmu-mir-28a, hsa-mir-130b, hsa-mir-367, hsa-mir-372, hsa-mir-378a, mmu-mir-378a, hsa-mir-340, hsa-mir-151a, mmu-mir-466a, mmu-mir-467a-1, hsa-mir-505, hsa-mir-506, mmu-mir-367, hsa-mir-92b, hsa-mir-548a-1, hsa-mir-548b, hsa-mir-548a-2, hsa-mir-548a-3, hsa-mir-548c, hsa-mir-648, hsa-mir-548d-1, hsa-mir-548d-2, hsa-mir-421, hsa-mir-151b, hsa-mir-1271, hsa-mir-378d-2, mmu-mir-467b, mmu-mir-297b, mmu-mir-505, mmu-mir-297a-3, mmu-mir-297a-4, mmu-mir-297c, mmu-mir-421, mmu-mir-466b-1, mmu-mir-466b-2, mmu-mir-466b-3, mmu-mir-466c-1, mmu-mir-466e, mmu-mir-466f-1, mmu-mir-466f-2, mmu-mir-466f-3, mmu-mir-466g, mmu-mir-466h, mmu-mir-467c, mmu-mir-467d, mmu-mir-92b, mmu-mir-466d, hsa-mir-297, mmu-mir-467e, mmu-mir-466l, mmu-mir-669g, mmu-mir-466i, mmu-mir-466f-4, mmu-mir-466k, mmu-mir-467f, mmu-mir-466j, mmu-mir-467g, mmu-mir-467h, mmu-mir-1195, hsa-mir-548e, hsa-mir-548j, hsa-mir-1285-1, hsa-mir-1285-2, hsa-mir-1289-1, hsa-mir-1289-2, hsa-mir-548k, hsa-mir-1299, hsa-mir-548l, hsa-mir-1302-1, hsa-mir-1302-2, hsa-mir-1302-3, hsa-mir-1302-4, hsa-mir-1302-5, hsa-mir-1302-6, hsa-mir-1302-7, hsa-mir-1302-8, hsa-mir-548f-1, hsa-mir-548f-2, hsa-mir-548f-3, hsa-mir-548f-4, hsa-mir-548f-5, hsa-mir-1255a, hsa-mir-548g, hsa-mir-548n, hsa-mir-548m, hsa-mir-548o, hsa-mir-1268a, hsa-mir-548h-1, hsa-mir-548h-2, hsa-mir-548h-3, hsa-mir-548h-4, hsa-mir-548p, hsa-mir-548i-1, hsa-mir-548i-2, hsa-mir-548i-3, hsa-mir-548i-4, hsa-mir-1255b-1, hsa-mir-1255b-2, mmu-mir-1906-1, hsa-mir-1972-1, hsa-mir-548q, mmu-mir-466m, mmu-mir-466o, mmu-mir-467a-2, mmu-mir-467a-3, mmu-mir-466c-2, mmu-mir-467a-4, mmu-mir-466b-4, mmu-mir-467a-5, mmu-mir-466b-5, mmu-mir-467a-6, mmu-mir-466b-6, mmu-mir-467a-7, mmu-mir-466b-7, mmu-mir-467a-8, mmu-mir-467a-9, mmu-mir-467a-10, mmu-mir-466p, mmu-mir-466n, mmu-mir-466b-8, hsa-mir-3116-1, hsa-mir-3116-2, hsa-mir-3118-1, hsa-mir-3118-2, hsa-mir-3118-3, hsa-mir-548s, hsa-mir-378b, hsa-mir-466, hsa-mir-548t, hsa-mir-548u, hsa-mir-548v, hsa-mir-3156-1, hsa-mir-3118-4, hsa-mir-3174, hsa-mir-3179-1, hsa-mir-3179-2, hsa-mir-3179-3, hsa-mir-548w, hsa-mir-3156-2, hsa-mir-3156-3, hsa-mir-548x, mmu-mir-3470a, mmu-mir-3470b, mmu-mir-3471-1, mmu-mir-3471-2, hsa-mir-378c, hsa-mir-1972-2, hsa-mir-1302-9, hsa-mir-1302-10, hsa-mir-1302-11, mmu-mir-1906-2, hsa-mir-3683, hsa-mir-3690-1, hsa-mir-548y, hsa-mir-548z, hsa-mir-548aa-1, hsa-mir-548aa-2, hsa-mir-548o-2, hsa-mir-1268b, hsa-mir-378d-1, hsa-mir-378e, hsa-mir-548h-5, hsa-mir-548ab, hsa-mir-378f, hsa-mir-378g, hsa-mir-548ac, hsa-mir-548ad, hsa-mir-548ae-1, hsa-mir-548ae-2, hsa-mir-548ag-1, hsa-mir-548ag-2, hsa-mir-548ah, hsa-mir-378h, hsa-mir-548ai, hsa-mir-548aj-1, hsa-mir-548aj-2, hsa-mir-548x-2, hsa-mir-548ak, hsa-mir-548al, hsa-mir-378i, hsa-mir-548am, hsa-mir-548an, mmu-mir-28c, mmu-mir-378b, mmu-mir-28b, hsa-mir-548ao, hsa-mir-548ap, mmu-mir-466q, hsa-mir-548aq, hsa-mir-548ar, hsa-mir-548as, hsa-mir-548at, hsa-mir-548au, hsa-mir-548av, hsa-mir-548aw, hsa-mir-548ax, hsa-mir-378j, mmu-mir-378c, mmu-mir-378d, hsa-mir-548ay, hsa-mir-548az, hsa-mir-3690-2, mmu-mir-290b, hsa-mir-548ba, hsa-mir-548bb, hsa-mir-3179-4, mmu-mir-466c-3, hsa-mir-548bc, mmu-mir-1271
Exceptions to this were hsa-mir-130b and hsa-mir-648 that we classified as NRdmiRs, and hsa-mir-659 that was classified as a PRdmiR. [score:1]
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