sort by

14 publications mentioning hsa-mir-3648-1

Open access articles that are associated with the species Homo sapiens and mention the gene name mir-3648-1. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

1
[+] score: 197
Since this miRNA is also found to be upregulated in several other diseases such as HCC, RCC and UT-UC, the downregulation of APC2 by miR-3648 might be associated with these diseases. [score:11]
In order to identify potential targets of miR-3648, we used three algorithms i. e. Targetscan, miRDB and miRWalk, and 13 target genes in common were identified [36, 37, 38] (Figure 3A). [score:7]
When miR-3648 was overexpressed, both the mRNA and protein levels of APC2 were downregulated (Figure 3D). [score:6]
The increased levels of miR-3648 then suppressed the expression of APC2, a negative regulator of cell proliferation and Wnt signaling pathway. [score:6]
We demonstrate that expression level of pri-miR-3648 along with mature miR-3648 is up-regulated during ER stress (Figure 2F). [score:6]
These results showed that APC2 was the only miR-3648 target among the 13 predicted genes, and it was a direct target with miR-3648 binding sites in its 3′ UTR. [score:6]
Both the APC2 mRNA and protein levels were further downregulated when miR-3648 was overexpressed in ER stressed cells (Figure 4B). [score:6]
It is interesting to notice that among the 13 predicted targets of miR-3648, only APC2 is the direct target of miR-3648 (Figure 3). [score:6]
These results revealed that elevated levels of miR-3648 suppressed the expression of APC2 in cells under ER stress. [score:5]
We checked the endogenous expression of miR-3648 in different human cell lines and tissues, and found this miRNA to be expressed in all the tested cell lines and tissues (Figure 1A,B). [score:5]
In this study, we also find increased expression level of target genes of Wnt/β-catenin signaling pathway (Figure 4E), and our data regarding miR-3648 and APC2 add a novel link between ER stress and Wnt/β catenin signaling in human cells. [score:5]
The tumor suppressor APC2 was found to be the major target of miR-3648 in ER stressed cells. [score:5]
Adenomatous polyposis coli 2 (APC2) was found to be the direct target of miR-3648. [score:4]
Upregulation of miR-3648 Increased Cell Proliferation. [score:4]
By targeting APC2, miR-3648 played critical roles in regulating cell proliferation under ER stressed condition. [score:4]
In this study, we identified miR-3648, a human specific miRNA, to be upregulated in cells under ER stress. [score:4]
We found that miR-3648, a human specific microRNA, was upregulated upon ER stress. [score:4]
Sequencing data previously generated in our lab showed miR-3648 to be upregulated in ER stress [26]. [score:4]
2.3. miR-3648 Directly Targeted the 3′ UTR of APC2. [score:4]
Further study is required to explore the mechanism of transcriptional regulation of miR-3648 expression during ER stress. [score:4]
These studies along with our study indicate that miR-3648 may be a tumor promoting miRNA, and is upregulated in multiple conditions that trigger ER stress, as ER stress can also be induced during viral infections [42]. [score:4]
Our findings demonstrated that ER stress mediated induction of miR-3648, which then downregulated APC2 and increase cell proliferation. [score:4]
These data indicated that miR-3648 might play physiological roles in many human cells, and its expression might be regulated in conditions such as ER stress. [score:4]
miR-3648 is also shown to be up-regulated in multiple high throughput researches in conditions such as Japanese Encephalitis Virus infection in microglia cells, HBV -positive HCC cells, and also in Renal cell carcinoma (RCC) and Upper tract carcinoma (UT-UC) [39, 40, 41]. [score:4]
We demonstrated that levels of APC2 were downregulated when miR-3648 was induced. [score:4]
In an effort to identify microRNAs upregulated upon ER stress, we noticed that levels of mature miR-3648 were increased when cells were treated with TG, a drug commonly used to induce ER stress, in HEK293T cells (Figure 2A). [score:4]
Conversely, when the cells were transfected with miR-3648 antagomir (ant3648), both the mRNA and protein levels of APC2 were upregulated (Figure 3E). [score:4]
Cell proliferation was similarly increased in cells with miR-3648 overexpression (Figure 5E,F). [score:3]
Many human specific miRNAs such as miR-3648 have been identified, however, most of them have no identified targets or functionality yet [32, 47]. [score:3]
Conversely, when miR-3648 was overexpressed, APC2 levels were decreased and the cell growth increased. [score:3]
Thus far, our findings suggested that miR-3648 was induced, and then APC2 was suppressed, in ER stressed cells. [score:3]
Luciferase assays confirmed that miR-3648 could regulate APC2 by targeting the 3′ UTR of APC2 in ER stressed cells (Figure 4D). [score:3]
Expression of miR-3648 in Human Cell Lines and Tissues. [score:3]
Suppression of miR-3648 Decreased Cell Proliferation. [score:3]
Western blots were performed from the cells transfected with miR-3648 overexpressing plasmids or ant-3648 after 48 h. While Western blots for TG treatment cells were performed at the indicated times post treatments, wor Western blots, samples were separated on 10% SDS–PAGE gels and then transferred to PVDF membranes (Millipore, Billerica, MA, USA). [score:3]
Inhibition of miR-3648 increased APC2 levels and decreased the cell proliferation. [score:3]
Further, we mutated all the three predicted binding sites of miR-3648 within the 3′ UTR of APC2, and the suppressive effect of miR-3648 was then abolished (Figure 3C). [score:3]
We then suppressed the function of miR-3648 by applying the miR-3648 specific antagomir (ant3648) (Figure 6). [score:3]
APC2 is identified as the target of miR-3648 in ER stressed cells. [score:3]
To examine this, we overexpressed miR-3648 in HeLa and HEK293T cells (Figure 5). [score:3]
miR-3648 is expressed in essentially all cells and tissues examined (Figure 1), is induced, and plays critical roles in ER stressed cells. [score:3]
APC2 Was Regulated by miR-3648 under ER Stress. [score:2]
We observed cells overexpressed with miR-3648 formed significantly more colonies in cells compared to control group (Figure 5A,B). [score:2]
Levels of pri-miR-3648 and mature miR-3648 were significantly increased with TG treatment (Figure 2F). [score:1]
miR-3648 is a human specific miRNA, and no ortholog exists in great apes and the other mammals [32]. [score:1]
Roles of miR-3648 in ER stress and other forms of cellular stress in human cells also deserve further study. [score:1]
Overexpression of miR-3648 could also enhance the anchorage-independent growth (examined with soft agar assays) as compared to control group (Figure 5C,D). [score:1]
Similarly miR-3648 was induced when HEK293T cells were treated with Tunicamycin (TM), another drug that can induce ER stress (Figure 2C). [score:1]
To know at which stage the induction of miR-3648 happened, we examined levels of pri-miR-3648 [35] (Figure 2F). [score:1]
For the functional analysis of miR-3648, partial segments of the mRNA 3′ UTR containing the miR-3648 binding sequences of APC2, CCNF, SKI, SGTA, INPP51, SLC12A5, UPF1, LPL, HMHA1, LRFN1, H2AFX, FOXD3 and ATF5 were PCR amplified from cDNA prepared from RNA of HEK293T cells. [score:1]
We also observed this induction of miR-3648 in HeLa cells treated with TG (Figure 2D). [score:1]
HEK293T cells (1 × 10 [6]) were transfected with 1μg of pmR-mCherry-miR-3648 or empty vector control, 1 μg of pGL3 Control Vector carrying the corresponding 3′ UTR and 10 ng pRL-TK renilla plasmid. [score:1]
Our study showed that the human specific miR-3648 was induced at the transcriptional level by ER stress. [score:1]
Conversely, miR-3648 antagomir significantly increased the APC2 mRNA and protein levels in ER stressed cells (Figure 4C). [score:1]
Therefore, miR-3648 might play roles in tumorigenesis, especially in the context of ER stress. [score:1]
These results demonstrated that levels of mature miR-3648 increased in cells under ER stress, and it was highly possible due to the transcriptional activation of pri-miR-3648. [score:1]
To investigate whether these decreases of APC2 levels in ER stressed cells were due to increases in miR-3648 levels (Figure 2 and Figure 3), we performed experiments to overexpress or block (with antagomir) miR-3648 in cells under ER stress (Figure 4B,C). [score:1]
We next examined miR-3648 levels with Northern blots, and mature miR-3648 was significantly increased with TG treatment for 8 h (Figure 2E). [score:1]
The relative luciferase activity of reporter with APC2 3′ UTR was significantly repressed by miR-3648, while no effect was observed on the luciferase activity for all the other 3′ UTR reporters (Figure 3B). [score:1]
2.2. miR-3648 Was Induced by the ER Stress. [score:1]
[1 to 20 of 60 sentences]
2
[+] score: 21
Among the 63 upregulated and 49 downregulated miRNAs in both the CP and CLP plasma samples, six miRNAs, namely miR-340–5p, miR-877–5p, miR-3648, miR-1260a, miR-494–3p, and miR-1304–3p, were selected for expression validation (Table 3). [score:9]
Relative expression level (2 [−ΔΔCt]) of miR-340-5p, miR-877-5p, miR-3648, miR-1260a, miR-494-3p, and miR-1304-3p expression in the plasma of cleft palate patients (n =16), cleft lip with cleft palate patients (n = 33) and controls (n = 8) (Mann-Whitney U test). [score:5]
The results showed that three miRNAs, miR-340–5p, miR-877–5p and miR-3648, were significantly upregulated in both the CP and CLP plasma samples (Figure 2). [score:4]
Six miRNAs, namely miR-340–5p, miR-877–5p, miR-3648, miR-1260a, miR-494–3p, and miR-1304–3p, were found to be differentially expressed in both the NSCP and NSCLP plasma samples. [score:3]
[1 to 20 of 4 sentences]
3
[+] score: 19
Flow cytometry analysis showed that the number of βIII-tubulin -positive cells was significantly decreased in cells overexpressing miR-663 (Figures 3c and d), but not in those overexpressing miR-3648 or miR-3687 (Supplementary Figures S3a and b). [score:5]
After overexpression of AICD, the expression levels of miR-663 significantly increased, and those of both miR-3648 and miR-3687 were significantly decreased (Figure 2f). [score:5]
To determine which of the AICD-regulated miRNAs are involved in inhibiting neuronal differentiation, we transfected molecular mimics of miR-663, miR-3687 or miR-3648 into hNSCs. [score:4]
As the binding sites for mir-663, mir-3648 and mir-3687 were situated near to the SSS of these miRNAs, the embedded regions were scanned using ChIP in both AICD -overexpressed and wild-type hNSCs. [score:3]
The mir-3648 and mir-3687 were clustered together in the genome, and the index of enrichment was significantly increased at −247 and +206 bp from the mir-3648 SSS, but not at more distant regions or gapdh promoter region (Figure 2h). [score:1]
Thus, these data demonstrate that AICD interacts with the chromatin regions of mir-3648, mir-3687, let-7a-1, mir-663, mir-3910, mir-193a and mir-595. [score:1]
[1 to 20 of 6 sentences]
4
[+] score: 11
Other miRNAs from this paper: hsa-mir-21, hsa-mir-146a, hsa-mir-155, hsa-mir-4741, hsa-mir-3648-2
Other induced genes for feedback repressors of the initial signaling cascade include the protein tyrosine kinase LYN, multiple members of the TRIM family of E3 ubiquitin ligases which promote degradation of signaling molecules (TRIM5, TRIM10, TRIM25, TRIM35, TRIM36, TRIM38), the TRAF inhibitor TANK, multiple inhibitor microRNAs (notably miR146A, miR155, miR21, miR3648, miR4741), IER3, each of the GADD45 family members, which amongst many other targets, probably inhibit p38 MAP kinases [64], the caspase inhibitor TNFAIP8 and the transcription factor ATF3 [28]. [score:11]
[1 to 20 of 1 sentences]
5
[+] score: 11
Consistent upregulation across 48 h pi was observed with miR-3648, miR-3687, miR-129-5p, miR-572, and two-way ANOVA confirmed that infection is the main factor in miRNAs deregulation as their expression increased along with increasing viral load (P < 0.001) (Fig. 3A–D). [score:7]
As shown in Fig. 3J, the expression of miR-3648, miR-3687, miR-129-5p, miR-572, increased with increased MOI used for initial infection in human microglial cells. [score:3]
The results of qPCR analysis of (A) miR-3648, (B) miR-3687 (C) miR-572, (D) miR-129-5p, (E) miR-197-3p, (F) miR-145-5p, (G) miR-374b-5p, (H) miR-26b-5p, (I) miR-149-5p, at three different time points are presented. [score:1]
[1 to 20 of 3 sentences]
6
[+] score: 8
Other miRNAs from this paper: hsa-mir-1247, hsa-mir-4285, hsa-mir-3648-2
PCNXL3 was reported to be one of the top 20 genes with the highest correlations with colon adenocarcinoma [42], MIR4285 and MIR3648 were shown to be differentially expressed in colon adenomas [43, 44], and MiR1247 as a potential tumor suppressive gene [45]. [score:5]
Top 10 hyper-methylated DMRs for Family/control pair are listed in Supplementary Table 3, the annotated genes are PCNXL3, RFPL2, LOC729176, TONSL, NLGN2, GNAS, TPRX1, EGFLAM, PRKAR1B, and MIR3648 (genes underlined are overlapping with genes found for the Cancer/control pair in Table 3). [score:1]
Interestingly, among those top 10 hyper- and hypo- methylated genes, several of them are overlapping with those in Cancer/control pair, including PCNXL3, TONSL, NLGN2, GNAS, MIR3648, SLC2A3 (GLUT3) and SLC2A1 (GLUT1). [score:1]
Table 3 lists the top 10 most significant hyper-methylated DMRs (distance to transcription start site [TSS] were from -1,000 to +1,000 base-pair [bp] DNA) for Cancer/control pair, and the annotated genes are PCNXL3, MIR4285, NLGN2, MIR3648, HOXA4, CLDN23, TONSL, GNAS, TUBB8 and MIR1247. [score:1]
[1 to 20 of 4 sentences]
7
[+] score: 7
According to previous reports, rRNA-contained miRNAs such as miR-663, miR-1275, miR-3648, miR-3656, miR-3687, miR-4417, and miR-4516 are associated with tumor suppression, carcinomas, neuronal differentiation, breast cancer, breast cancer/neuronal differentiation, breast cancer, and regulation of signal transducer and activator of transcription 3, respectively [103– 108]. [score:4]
Among these detected miRNAs, miR-1268a, miR-3648, miR-3687, miR-4508, and miR-6724 were originated in rDNA containing chromosomes, Chr 15, Chr 21, Chr 21, Chr 15, and Chr 21, respectively. [score:1]
Subsequently, seventeen RNA alignments identical to human mature miRNAs, namely, miR-663a, miR-663b-3p, miR-1268a, miR-1268b, miR-1275, miR-3648, miR-3656-3p, miR-3687-3p, miR-4417, miR-4466, miR-4488, miR-4492-3p, miR-4508, miR-4516, miR-4532, miR-6087, and miR-6724, were detected from the human rRNA sequences (Table 1). [score:1]
As a result, passenger strands of miR-663a, miR-3648, miR-3687, miR-6087, and miR-6724 were found nearby their guide strands (Figure 1(a)). [score:1]
[1 to 20 of 4 sentences]
8
[+] score: 4
Only four conserved target genes were predicted for this miRNA, which may indicate either little functional relevance or a high degree of specialisation for miR-3648. [score:3]
The largest number of human-specific substitutions found in one miRNA was seven, in hsa-mir-3648, that also contained three substitutions in the chimpanzee lineage. [score:1]
[1 to 20 of 2 sentences]
9
[+] score: 3
Altogether, 20 high confidence expressed miRNA were identified and the presence of miR1244 and miR3648/3687 precursors in the EVs was further validated by PCR (Supplementary Fig.   S5). [score:3]
[1 to 20 of 1 sentences]
10
[+] score: 3
Four mature miRNAs (hsa-miR-3124-5p, hsa-miR-3647-3p, hsa-miR-3647-5p, hsa-miR-3648) were excluded from the analysis because each of them has no predicted target gene according to this tool. [score:3]
[1 to 20 of 1 sentences]
11
[+] score: 2
Other miRNAs from this paper: hsa-mir-3648-2
Fungal insertions Geotrichum Intergenic- 560 Kb upstream of the GABRG1 gene (chr4) Pleistophora Intron of ITCH (chr20) Intron of MAGI1 (chr 3) Phialophora Intron of ZNRF2 (chr7) Rhodotorula Intron of CADPS2 (chr7) Parasitic insertions Strongyloides Exon of ZNF383 (chr19) Intron of LNP1 (chr3) Intergenic- downstream of SLC10A2 (chr13) Intron of SPECC1 (chr17) Contracaecum Exon of RHD (chr1) Trichinella intron of AKAP1 (chr17) Intron of EPS15L1 (chr19) Intergenic- 353 Kb upstream of NRG3 (chr10) Echinococcus Intron of ATRX (chrX) 21 Kb upstream of FGFR2 Prosthodendrium Intron of USP32 (chr17) Intergenic region- 37 Kb upstream of Lyn gene Hymenolepis Downstream of MIR3648 (chr21) Diphyllobothrium Intergenic- 106 Kb upstream of TRIM49B (chr9) in the ncRNA ANKRD30BL gene JC Polyoma (JC) viral genomic integration was observed in human chromosomes 1, 2, 5, 6, 10, 13, 15, 16, 17, 19, X and Y (Fig.   6a). [score:1]
Fungal insertions Geotrichum Intergenic- 560 Kb upstream of the GABRG1 gene (chr4) Pleistophora Intron of ITCH (chr20) Intron of MAGI1 (chr 3) Phialophora Intron of ZNRF2 (chr7) Rhodotorula Intron of CADPS2 (chr7) Parasitic insertions Strongyloides Exon of ZNF383 (chr19) Intron of LNP1 (chr3) Intergenic- downstream of SLC10A2 (chr13) Intron of SPECC1 (chr17) Contracaecum Exon of RHD (chr1) Trichinella intron of AKAP1 (chr17) Intron of EPS15L1 (chr19) Intergenic- 353 Kb upstream of NRG3 (chr10) Echinococcus Intron of ATRX (chrX) 21 Kb upstream of FGFR2 Prosthodendrium Intron of USP32 (chr17) Intergenic region- 37 Kb upstream of Lyn gene Hymenolepis Downstream of MIR3648 (chr21) Diphyllobothrium Intergenic- 106 Kb upstream of TRIM49B (chr9) in the ncRNA ANKRD30BL gene JC Polyoma (JC) viral genomic integration was observed in human chromosomes 1, 2, 5, 6, 10, 13, 15, 16, 17, 19, X and Y (Fig.   6a). [score:1]
[1 to 20 of 2 sentences]
12
[+] score: 1
Location Human Gene or comment chr1:10,291,843-10,314,721 RNU6-1,2,7,8,9 intronic of KIF1B chr1:91,344,238-91,430,371 HFM1 intronic chr2:132,234,625-132,276,521 ANKRD30BL intronic (near MIR663B) chr8:69,676,805-69,703,480 SLCO5A1 intronic chr21:8,183,959-8,252,641 NR_038958 and 28 S RNA intronic (near MIR3648 and MIR663A) chr21:8,393, 229-8,410,398 NR_038958 intronic and 28 S RNA exonic chr21:8,429,258-8,463,598 28 S RNA 45 S RNA exonic Location Plasmodium Gene or comment many nearly all rRNA genes Supercontig_1.3:841,093–845,256 T complexe protein PFC0900w Supercontig_1.4:520,965-530,102 tRNA-Glu1 Supercontig_1.7:716,587–734,017 tRNA-Asp1 Supercontig_1.11:126,943-135,040 near PF11_0040-1 (3′utr?) [score:1]
[1 to 20 of 1 sentences]
13
[+] score: 1
Other miRNAs from this paper: hsa-mir-3648-2
Therefore of the 17 ZSCAN5B DEGs identified as nearest to HEK-293 ZSCAN5B ChIP peaks, only eight genes - HES7, TRIM7, NDUFS7, TIA1, C17ORF59, C16ORF13, GEMIN7, MIR3648 - were found within 5 kb of the peaks. [score:1]
[1 to 20 of 1 sentences]
14
[+] score: 1
The expressions of 14 miRNAs [i. e., human chromosome (hsa)-let-7c, hsa-mir-125b-2, hsa-mir-155, hsa-mir-3118, hsa-mir-3156, hsa-mir-3197, hsa-mir-3648, hsa-mir-3687, hsa-mir-4327, hsa-mir-4759, hsa-mir-4760-3p, hsa-mir-548x, hsa-mir-802, and hsa-mir-99a] encoded by chromosome 21 were evaluated; u6-snRNA was used as the control sample for normalization. [score:1]
[1 to 20 of 1 sentences]