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54 publications mentioning hsa-mir-520d

Open access articles that are associated with the species Homo sapiens and mention the gene name mir-520d. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

1
[+] score: 90
Over -expression of miR-520d, miR-101, miR-140, miR-485 and miR-448 in different T-ALL cell lines resulted in down-regulation of TAL1 transcript (Figure 4A) and/or protein (Figure 4B-4C) expression levels in a range of 20-60%. [score:8]
A. Western blot and densitometric and analysis of TAL1 expression in CCRF-CEM cells upon nucleofection with microRNA inhibitors (si101 against hsa-miR-101 or si520d against hsa-miR-520d-5p), a siRNA against TAL1 (siT1) or a non -targeting siRNA control (siNT). [score:7]
Figure 5 A. Western blot and densitometric and analysis of TAL1 expression in CCRF-CEM cells upon nucleofection with microRNA inhibitors (si101 against hsa-miR-101 or si520d against hsa-miR-520d-5p), a siRNA against TAL1 (siT1) or a non -targeting siRNA control (siNT). [score:7]
The mutation of a putative binding site for miR-520d-3p in the 3′UTR (Figure 2C) increased the luciferase expression by 15% when compared with the non-mutated 3′UTR (Figure 3C), suggesting that the down-regulation of the reporter for miR-520d was partly dependent on the 3p form. [score:6]
Ectopic expression of miR-520d, -101, -140, -485 and -448 down-regulates endogenous TAL1 mRNA and protein levels in T-ALL cell lines. [score:6]
For miR-101 or miR-520d-5p knockdown, 2μM of miRCURY LNA™ microRNA Inhibitors (Exiqon) and non -targeting control were used. [score:6]
We verified that inhibition of miR-520d-5p and miR-101 rescued endogenous TAL1 protein expression by 20 to 40% on average (Figure 5A-5B). [score:5]
A. Expression of miR-101, miR-520d-5p, miR-140-5p and miR-448 was determined by qRT-PCR and normalized to SNORD38B expression in TAL1 -positive (SUP-T1, CCRF-CEM, TAIL7, PF-382) and TAL1 -negative (HPB-ALL, P12-ICHIKAWA, TALL-1) T-ALL human cell lines. [score:5]
Figure 6 A. Expression of miR-101, miR-520d-5p, miR-140-5p and miR-448 was determined by qRT-PCR and normalized to SNORD38B expression in TAL1 -positive (SUP-T1, CCRF-CEM, TAIL7, PF-382) and TAL1 -negative (HPB-ALL, P12-ICHIKAWA, TALL-1) T-ALL human cell lines. [score:5]
While we have not explored this possibility in the current manuscript, we note that even if such transcripts prevail in T-ALL cases, the most upstream canonical poly-adenylation site would only protect the MRE corresponding to miR-520-3p, miR-140-3p (both of which we showed to have no effect on reporter expression recovery upon mutagenesis assays) and the 4th MRE for miR-520-5p, which we showed that, together other two MREs for miR-520-5p, is not sufficient to recover the reporter expression. [score:4]
Down-regulation mediated by these miRNAs in the TAL1 transcript was observed for miR-520d, miR-101, miR-140 and miR-448 in PF-382 cells and for miR-520d and miR-140 in SUP-T1 cells (Figure 4A). [score:4]
Figure 2Details of binding of A. miR-101; B. miR-520d-5p and D. miR-140-5p to TAL1 3′UTR are depicted according to DianaMicroT [71] target prediction algorithm. [score:3]
Therefore, miR-520d-5p and miR-101 affect TAL1 mostly at the level of translation in T-ALL cells. [score:3]
The triple mutants in TAL1 3′UTR did not restore the luciferase expression in the presence of miR-520d (Figure 3B). [score:3]
Interestingly, miR-101 [20, 43- 52], miR-140-5p [53- 56], miR-520-5p [57], and miR-485-5p [58- 60], are all reported as putative tumor suppressors in different cancers. [score:3]
Inhibition of miR-520d-5p and miR-101 increases endogenous TAL1 protein levels in T-ALL cells. [score:3]
The miR-520d precursor can give rise to two mature forms of the microRNA, the 5p from the 5′ arm of the hairpin and 3p from the 3′ arm of the hairpin, both expressed by miR-Vec vectors. [score:3]
Details of binding of A. miR-101; B. miR-520d-5p and D. miR-140-5p to TAL1 3′UTR are depicted according to DianaMicroT [71] target prediction algorithm. [score:3]
For further analysis we selected microRNAs that significantly lowered the luciferase expression in 25-50%: miR-101, miR-520d-5p, miR-140-5p, miR-448 and miR-485-5p (see Figure 2 for miRNA binding details). [score:3]
Results were normalized to scramble (SCR) miRNA on WT TAL1 3′UTR: A. miR-101, B, C. miR-520d, and D, E. miR-140. [score:1]
The miR-520d-5p has four predicted binding sites in the 3′UTR (Figure 2B) and we were able to mutate three of them. [score:1]
The miRNAs miR-520-3p C. and miR-140-3p E. are not predicted to bind to TAL1 3′UTR, nevertheless the putative MRE were mutated as depicted. [score:1]
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2
[+] score: 69
↓: injection of complex (once a week); ▲: atelocollagen alone; ●: scramble/atelocollagen; ■: miR-520d-5p/atelocollagen (cases with suppressive growth); □: miR-520d-5p/atelocollagen (cases with tumor disappearance); ✝: mice were sacrificed; CI: confidence intervalAmong HLF tumors, the average suppression rates of tumor size in the subcutaneous, intraperitoneal, and systemic (metastasis) mo dels were 92.7 %, 75.0 % (6/8) and 100 % (8/8), respectively (Table  1). [score:5]
520d/HMV-I tumors significantly expressed 520d-5p (*, P < 0.05), and 520d/HLF tumors tended to express miR-520d-5p (P = 0.051). [score:5]
Although the tumors that were resected at the end of the observation period no longer demonstrated suppressed growth, we examined the expression level of miR-520d-5p in the resected tumors. [score:5]
↓: injection of complex (once a week); ▲: atelocollagen alone; ●: scramble/atelocollagen; ■: miR-520d-5p/atelocollagen (cases with suppressive growth); □: miR-520d-5p/atelocollagen (cases with tumor disappearance); ✝: mice were sacrificed; CI: confidence interval Among HLF tumors, the average suppression rates of tumor size in the subcutaneous, intraperitoneal, and systemic (metastasis) mo dels were 92.7 %, 75.0 % (6/8) and 100 % (8/8), respectively (Table  1). [score:5]
We previously demonstrated that hsa-miR-520d-5p can convert cancer cells into induced pluripotent stem cells (iPSCs) or mesenchymal stem cells (MSCs) via a demethylation process and p53 upregulation in vivo. [score:4]
In the case of miR-520d-5p, which can convert undifferentiated hepatoma cells (HLF) to a benign or normal status in vivo [27], available bioinformatics predict that it has greater than 8000 target genes. [score:3]
In the present study, we assessed the tumor-suppressive effect of miR-520d-5p on undifferentiated melanoma cells (HMV-I) in vitro and attempted to examine the therapeutic effect of the miRNA on two cell lines (HLF or HMV-I) using atelocollagen as a DDS carrier biomaterial. [score:3]
After we confirmed miR-520d expression (Fig.   2b), DNA content, analyzed by flow cytometry, revealed a shift toward homogeneous proliferation in the S phase, as described for the HLF cells in our previous report [27] (Fig.   2c). [score:3]
miR-520d-5p induced the expression of Nanog in HMV-I cells (x100 magnification) (bottom). [score:3]
In this study, we first attempted to examine the tumor suppressive effect of miR-520d-5p using atelocollagen with subcutaneous injection. [score:3]
To examine the effects of miR-520d-5p overexpression, we transfected pMIRNA1-miR-520d-5p/GFP (20 mg; System Biosciences, Mountain View, CA, USA) into 293FT cells (5 × 10 [6] cells/10-cm culture dish). [score:3]
Genes were chosen from those with altered expression levels in response to miR-520d-5p induction and silencing. [score:3]
a miR-520d-5p expression was examined in HLF (n = 5) and HMV-I (n = 7) tumors resected after 520d/atelocollagen treatment. [score:3]
The arrow shows the murine muscle region without human SIX1 staining (bottom left) As we reported previously [27], HLF could be converted to a benign or normal status by miR-520d-5p via a stemness -mediated process. [score:1]
Thus, miR-520d may be an interesting molecule whose mechanism should be clarified. [score:1]
DNA content was analyzed with a flow cytometer; the cells were assessed by approximately 20,000 collected events after the transfection of a pMIRNA1-miR-520d-5p/GFP clone and prior to EXPO32 ADC analysis software. [score:1]
Although miR-520d-5p completely penetrates all of the tumor cells in tumor tissues, viable cells persist after its delivery. [score:1]
HLF and HMV-I cells were infected with lentiviral particles that contained hsa-miR-520d-5p. [score:1]
Immunodeficient KSN/Slc mice were used to examine the anti-metastatic effects of miR-520d-5p or the transformation to normal status by miR-520d-5p (Fig.   1). [score:1]
As we reported previously [27], HLF could be converted to a benign or normal status by miR-520d-5p via a stemness -mediated process. [score:1]
The sequence of our prepared hsa-miR-520d-5p was 5′-cuacaaagggaagcccuuuc-3′ and 3′-uugauguuucccuucgggaaag-5′ (Fig.   1). [score:1]
Additionally, we have reported the non-tumorigenic effect of miR-520d-5p on normal human cells, including fibroblasts. [score:1]
Cells were assessed by approximately 20,000 collected events after the transfection of a pMIRNA1-miR-520d-5p/GFP clone using EXPO32 ADC analysis software. [score:1]
To identify the anti-cancer effects of miR-520d, we examined its effects on two cell lines (HLF or HMV-I) in vivo. [score:1]
The suppressive effect of miR-520d-5p on subcutaneous tumors and metastasis was calculated based on the data collected each week or the findings at the time of sacrifice (Additional file 3: Table S2 or Additional file 4: Table S3, respectively). [score:1]
Because miR-520d-5p did not appear to have any toxic effects on normal cells or cancer cells and did not induce tumorigenicity or malignant transformations in vivo [28], we examined the therapeutic effects of 520d-5p conjugated with atelocollagen as a drug delivery system (DDS) carrier on undifferentiated cancer cells using in vivo imaging. [score:1]
Cancer miR-520d-5p Xenograft mo del Therapeutic effect Mature miRNAs are endogenous, small, noncoding RNA (ncRNA) molecules that are 18 to 23 nucleotides in length and transcribed by RNA polymerase II. [score:1]
We used atelocollagen-conjugated miR-520d-5p (520d/atelocollagen) to confirm the possibility of a therapeutic effect on cancer cells. [score:1]
Mature miRNA (miR-520d-5p, 25 ng/μl) was quantified with the Mir-X™ miRNA qRT-PCR SYBR® kit (Takara Bio, Tokyo, Japan) according to the manufacturer’s instructions. [score:1]
Six-week-old immunodeficient mice were inoculated for in vivo study by miR-520d-5p transfection. [score:1]
The Mann-Whitney U-test was used for comparisons between the controls, the scrambled and/or the miR-520d-5p results with one observed variable. [score:1]
and miR-520d-5p were conjugated following the manufacturer’s instructions, and the resulting complex was injected into immunodeficient mice that were inoculated with cancer cells. [score:1]
An in vivo study using glioblastoma cells (T98G) treated with miR-520d-5p (520d/T98G). [score:1]
The miR-520d-5p/atelocollagen complex was injected into immunodeficient mice topically, intraperitoneally or systemically (Fig.   1). [score:1]
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3
[+] score: 66
We also found that the expression level of members of the two clusters, miR-520b and miR-302c, were negatively correlated with their targeted genes based on gene expression analysis We identified the expression patterns of miRNAs and gene transcripts in the undifferentiation of human embryonic stem cells; among the miRNAs that are highly expressed in undifferentiated embryonic stem cells, the miR-520 cluster may be closely involved in hES cell function and its relevance to chromatin structure warrants further study. [score:11]
To infer the function of these miRNAs, we predicted 2,436 targets for the miR-302 cluster and 4,691 targets for the miR-520 cluster by querying the public database miRNAMap 2.0, and 2,284 target genes were shared by both clusters suggesting functional similarity. [score:7]
Our results confirmed the recent report that majority of miRNA genes in hES cells were expressed from Chromosomes 19 and X [55] and demonstrated the significant upregulation of miR-520 cluster in hES cells. [score:6]
Among the hES signature miRNAs, the miR-520 cluster shared a similar expression pattern and seed sequence as the well known miR-302 family and targeted the same genes as the miR-302 family. [score:5]
Among the miRNAs upregulated in hES cells, we observed 7 miRNAs were located in the miR-302 cluster and 21 miRNAs were located in miR-520 cluster. [score:4]
The upregulation of miR-302 cluster and miR-520 cluster in hES cells suggests their ability to modulate local chromatin states which is necessary for stem cell pluripotency [58, 59]. [score:4]
In addition, we identified 12 other hES upregulated miRNAs in this cluster: miR-302a, miR-302b, miR-302c, miR-302d, miR-519b, miR-519c, miR-520a, miR-520b, miR-520c, miR-520d, miR-520e which share a consensus seed sequence: AAGUGC [24]. [score:4]
In addition, we identified 21 hES upregulated miRNAs that were co-localized in a cluster on chromosome 19, the miR-520 cluster, many of which shared consensus seed sequence with miR-302 family and which can be used as candidate biomarkers for pluripotency (Additional file 1). [score:4]
Along with the reports of miR-302 family on chromosome 4 [16, 17, 19, 25, 26], several groups have reported the expression of members of miR-520 cluster on chromosome 19 in hES cells [24, 26, 29]. [score:3]
The miR-302 cluster and miR-520 cluster target large groups of genes which share overlapping functions based on Gene Ontology (GO) analysis. [score:3]
Gene Ontology (GO) enrichment analysis confirmed that the inferred functions of miRNAs within the miR-302 and miR-520 clusters were overlapping based on their involvement in cell growth, negative regulation of cellular metabolic process, negative regulation of transcription, and small GTPase mediated signal transduction. [score:3]
Especially, members of the miR-302 cluster on chromosome 4 and miR-520 cluster on chromosome 19 were highly expressed in undifferentiated hES cells. [score:3]
To visualize the functions of these miRNA targeted genes, a binary (red indicate participate in the functional category and green indicate not) heatmap was used to indicate functional commonality among all miRNAs in miR-302 and miR-520 clusters. [score:3]
Figure 8 Sequence and GO analysis of the miR-302 cluster and miR-520 cluster. [score:1]
The members of the miR-302 and miR-520 clusters had similar sequences; they shared a consensus seed sequence: AAGUGC (panel A, seed sequence is highlighted by the purple rectangle). [score:1]
Besides these 9 miRNAs, we also identified 12 more miRNAs in this cluster; they were miR-515-5p, miR-517a, miR-517b, miR-517c, miR-519e, miR-520b, miR-520d, miR-520f, miR-520h, miR-521, miR-525-3p, and miR-526b*. [score:1]
Less is known about the function of the miR-520 cluster. [score:1]
In particular, miR-302a, miR-302b, miR-302c, miR-302d, miR-519b, miR-519c, miR-520a, miR-520b, miR-520c, miR-520d, and miR-520e had a consensus seed sequence: AAGUGC (Figure 8, panel A). [score:1]
Functional comparison of miR-302 cluster and miR-520 cluster. [score:1]
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4
[+] score: 37
MSC expression of the eight C19MC miRNAs could be grouped in three expression patterns: group A, which included miR-512-3p and -520c-3p, showed very low or undetectable expression in the MSCs; expression of the group B miR-520d-5p, 519b-3p and -524-5p was detected in at least one or both MSC cell lines, whereas miR-520f-3p, -517a-3p and -520g-3p in group C were all expressed all three MSC cell lines (Fig.   1b and Table  2). [score:11]
Despite en bloc and high-level C19MC expression in JEG-3 cells, only four of the eight miRNAs, namely miR-520d-5p of Group B as defined above for stem cell expression, and all three Group C miRNAs, miR-520f-3p, -517a-3p and -520g-3p, were shown to be expressed in the normal placenta cell line Hs799. [score:7]
However, construction of a Venn diagram showed that only 262 putative target genes are common between the miR-519 and miR-520 subfamilies in group I, indicating that the miR-519 and -520 subfamilies target different sets of genes. [score:5]
To obtain further supporting evidences on selective activation, expression of eight miRNAs spanning the C19MC cluster (Fig.   1a), but with different genomic structures, was selected for further experimentally verification; amongst the selected miRNAs, miR-512-3p is transcribed by the two miR-512-1 and-512-2 genes located at the 5’-end of the C19MC miRNA gene cluster; miR-520c-3p, -519b-3p and -520f-3p are single miRNA genes located between previously proposed exons; miR-524-5p and -517a-3p are two of three miRNA genes mapped on intron 18 and miR520d-5p and -520g-3p are two of four miRNAs mapped on intron 20 (Fig.   1a) [24]. [score:3]
The group I miR-519 subfamily also shares 262 putative target genes with the miR-302/-372 families, far fewer than the miR-520 subfamily (Fig.   3a, red box). [score:3]
However, the miR-520 and miR-302/372 families share a significant number of target genes (Fig.   3a) suggesting common biological functions. [score:3]
Notably, the miR-524-5p and -517a-3p and the miR520d-5p and -520g-3p couples are flanked by two proposed exons but belong to different expression groups B and C (Fig.   1a). [score:3]
The results showed that 1185 putative shared genes were obtained between the miR-520 and -302/372 families (Fig.   3a, blue box and Additional file 1: Table S1), suggesting that the miR-520 subfamily might share similar biological functions with the miR-302/372 family. [score:1]
Hence, it is highly likely that the group I miR-520 miRNAs may also contribute to reprogramming, as supported by the predicted involvement of miR-520 miRNAs in the reprogramming-related apoptosis and cell proliferation pathways (see Fig.   4 and below). [score:1]
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5
[+] score: 31
Tsukerman P Yamin R Sei del E Khawaled S Schmie del D MiR-520d-5p directly targets TWIST1 and downregulates the metastamiR miR-10bOncotarget. [score:9]
Importantly, miR-520-5p has previously been reported to inhibit expression of the EMT-related gene TWIST1 [38]. [score:5]
Overexpression of miR-520d-5p alone has been reported to successfully convert hepatoma cells into iPSC-like cells [15]. [score:3]
miR-524-5p, a C19MC member, is highly homologous to the reprogramming miR-520d-5p; we also reported that miR-524-5p was expressed in iPSCs but not mesenchymal stem cells (MSCs). [score:3]
It also seems likely that different miRNA -driven regulatory mechanisms and pathways may be involved in reprogramming normal somatic cells as opposed to cancer cells, as in the case of miR-520d-5p and hepatoma [15]. [score:2]
Despite a recent report on the involvement of miR-520d-5p (a member of the C19MC) in reprogramming [15], it is unclear if other C19MC miRNAs also contribute to inducing and regulating pluripotency. [score:2]
Since both C19MC members including miR-520d-5p and miR-524-5p are highly homologous in sequences and share the same seed sequence (Fig.   1a), the two miRNAs may share similar biological functions. [score:1]
Tsuno S Wang X Shomori K Hasegawa J Miura N Hsa-miR-520d induces hepatoma cells to form normal liver tissues via a stemness -mediated processSci Rep. [score:1]
Recent studies have indicated the ability of miR-520d-5p for converting cancer cells into iPSC-like cells [15, 24]. [score:1]
Ishihara Y Tsuno S Kuwamoto S Yamashita T Endo Y Hsa-miR-520d converts fibroblasts into CD105+ populationsDrugs RD. [score:1]
Our bioinformatics analysis revealed identical seed sequence and high degree of sequence homology between miR-524-5p and miR-520d-5p (Fig.   1a). [score:1]
a High degree of sequence homology (bold letters) between miR-524-5p and miR-520d-5p. [score:1]
Furthermore, miR-524-5p shares 19/20 nucleotides with miR-520d-5p (Fig.   1a), suggesting identical biological functions for both miRNAs. [score:1]
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6
[+] score: 27
Upregulation of miR-455-3p and miR-33a was found to be associated with chemosensitivity while upregulation of miR-224, miR-1236, and miR-520d-3p was associated with chemoresistance [21]. [score:7]
Interestingly, among the 736 miRNAs analyzed in the first study, upregulation of miR-455-3p and miR-33a was associated with chemosensitivity while upregulation of miR-224, miR-1236, and miR-520d-3p was associated with chemoresistance [21]. [score:7]
On the other hand, high expression of miR-224, miR-1236, and miR-520d-3p and low expression of miR-455-3p and miR-33a were found to be individually associated with unfavorable outcome and a score based on this five-miRNAs was proposed to predict the clinical outcome of DLBCL patients treated with R-CHOP regimen, independent from the IPI score [21]. [score:5]
In addition, a predictor score based on a signature of five miRNAs, among which high expression of miR-224, miR-1236, and miR-520d-3p and low expression of miR-455-3p and miR-33a were individually associated with unfavorable outcome, has been proposed to predict the clinical outcome of DLBCL patients, independent from the IPI score [21]. [score:5]
Five miRNAs were differentially expressed between both groups (miR-224, miR-1236, miR-520d-3p, miR-33a, and miR-455-3p) and were validated in an independent group of 133 patients. [score:3]
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7
[+] score: 20
Real-time PCR confirmed microarray analysis results: expression of miR-302a and miR-491-3p was up-regulated (Fig. 2) and miR-520d-3p and miR-383 was down-regulated (Fig. 2) in patients with NOA. [score:9]
Quantitative real-time PCR analysis confirmed microarray data: miR-302a and miR-491-3p was up-regulated and miR-520d-3p and miR-383 was downregulated in NOA patients. [score:7]
For example, one of the predicted target genes of miR-302a and miR-383 is MLH1, while miR-491-3p and miR-520d-3p is SCP1 and SCP3, respectively. [score:3]
To confirm the results obtained by microarray analysis, quantitative real-time RT-PCR analysis of normal and NOA testicular samples was performed for miR-302a, miR-491-3p, miR-520d-3p and miR-383. [score:1]
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8
[+] score: 14
The response graphs for miR-342, miR-520g and miR-520d* in relation to ER, PR and HER2/ neu status, respectively, are shown in Figure 4. Some miRNAs showed that with increased expression, the probability of receptor positivity increased; conversely, other miRNAs showed that with increased expression, the likelihood of the sample being classed as receptor -positive decreased. [score:5]
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]
Similarly, four miRNA transcripts (miR-520g, miR-377, miR-527-518a, miR-520f-520c) were identified that predicted tumour PR status with 100% accuracy, and HER2/ neu status was predicted with 100% accuracy by a signature of five miRNAs (miR-520d, miR-181c, miR-302c, miR-376b, miR-30e) (Table 3). [score:1]
Figure 4Response curves for miR-342, miR-520g and miR-520d. [score:1]
Response curves for (a) miR-342, (b) miR-520g and (c) miR-520d*. [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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9
[+] score: 13
Several miRNAs have been documented to directly inhibit TWIST1, including miR-1-1 [26], miR-33a [27, 28], miR-137 [29], miR-186 [30], miR-300 [31], miR-520d-5p [32], miR-539 [31], miR-543 [31], miR-675 [33], and miR-720 [34]. [score:4]
0168171.g007 Fig 7The expression levels of miR-1-1, miR-33a, miR-137, miR-186, miR-520d, miR-539, miR-543, miR-675, miR-720 in the breast cancer samples and the corresponding adjacent normal tissue samples (N = 101) were downloaded from the “The Cancer Genome Atlas” (TCGA) and the Broad GDAC Firehose data portal. [score:3]
The expression levels of miR-520d, miR-539, miR-543, and miR-675 in breast cancers were significantly lower than paired normal tissues (Fig 7). [score:3]
The expression levels of miR-1-1, miR-33a, miR-137, miR-186, miR-520d, miR-539, miR-543, miR-675, miR-720 in the breast cancer samples and the corresponding adjacent normal tissue samples (N = 101) were downloaded from the “The Cancer Genome Atlas” (TCGA) and the Broad GDAC Firehose data portal. [score:3]
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10
[+] score: 11
Other miRNAs from this paper: hsa-let-7b, hsa-mir-15a, hsa-mir-19a, hsa-mir-19b-1, hsa-mir-19b-2, hsa-mir-27a, hsa-mir-28, hsa-mir-30a, hsa-mir-100, hsa-mir-30c-2, hsa-mir-30d, hsa-mir-181a-2, hsa-mir-210, hsa-mir-181a-1, hsa-mir-221, hsa-mir-1-2, hsa-mir-15b, hsa-mir-30b, hsa-mir-122, hsa-mir-132, hsa-mir-141, hsa-mir-191, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-125a, hsa-mir-195, hsa-mir-200c, hsa-mir-1-1, hsa-mir-30c-1, hsa-mir-34b, hsa-mir-34c, hsa-mir-30e, hsa-mir-371a, hsa-mir-372, hsa-mir-373, hsa-mir-375, hsa-mir-151a, hsa-mir-429, hsa-mir-449a, hsa-mir-483, hsa-mir-193b, hsa-mir-520e, hsa-mir-520f, hsa-mir-520a, hsa-mir-520b, hsa-mir-520c, hsa-mir-520g, hsa-mir-520h, hsa-mir-548a-1, hsa-mir-548b, hsa-mir-548a-2, hsa-mir-548a-3, hsa-mir-548c, hsa-mir-548d-1, hsa-mir-548d-2, hsa-mir-449b, hsa-mir-151b, hsa-mir-320b-1, hsa-mir-320b-2, hsa-mir-891a, hsa-mir-935, hsa-mir-1233-1, hsa-mir-548e, hsa-mir-548j, hsa-mir-548k, hsa-mir-548l, hsa-mir-548f-1, hsa-mir-548f-2, hsa-mir-548f-3, hsa-mir-548f-4, hsa-mir-548f-5, hsa-mir-548g, hsa-mir-548n, hsa-mir-548m, hsa-mir-548o, hsa-mir-548h-1, hsa-mir-548h-2, hsa-mir-548h-3, hsa-mir-548h-4, hsa-mir-1275, hsa-mir-548p, hsa-mir-548i-1, hsa-mir-548i-2, hsa-mir-548i-3, hsa-mir-548i-4, hsa-mir-1973, hsa-mir-548q, hsa-mir-548s, hsa-mir-548t, hsa-mir-548u, hsa-mir-548v, hsa-mir-548w, hsa-mir-548x, hsa-mir-1233-2, hsa-mir-548y, hsa-mir-548z, hsa-mir-548aa-1, hsa-mir-548aa-2, hsa-mir-548o-2, hsa-mir-548h-5, hsa-mir-548ab, 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-548ai, hsa-mir-548aj-1, hsa-mir-548aj-2, hsa-mir-548x-2, hsa-mir-548ak, hsa-mir-548al, hsa-mir-548am, hsa-mir-548an, hsa-mir-371b, hsa-mir-548ao, hsa-mir-548ap, 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-548ay, hsa-mir-548az, hsa-mir-548ba, hsa-mir-548bb, hsa-mir-548bc
In patients with asthenozoospermia, two studies found that hsa-miR-27a [47, 56, 57], hsa-miR-548b-5p, hsa-miR-548c-5p and hsa-miR-548d-5p are up-regulated [47], while hsa-miR-34b-3p [47, 51], hsa-miR-520 h and hsa-miR-520d-3p are downregulated [47]. [score:7]
These miRNAs are expressed in spermatozoa and are involved in spermatogenesis (hsa-miR-34b-3p, hsa-miR-27a), embryonic development (hsa-miR-520 family) or in signaling pathways and human tumorigenesis (hsa-miR-548 family). [score:4]
[1 to 20 of 2 sentences]
11
[+] score: 9
In a Western blot analysis in the parental Panc1 cells 96 hours after transient transfection with these miRNAs, miR-520d-3p and miR-655, as well as miR-200b-3p, were confirmed to upregulate expression of the E-cadherin protein markedly, whereas only slight effects of other miRNAs were observed (Fig. 1D). [score:6]
Moreover, the relative fluorescence intensity of miR-655 was clearly higher than that of miR-520d-3p (Table 1), suggesting miR-655 to be a prime candidate for EMT-suppressive miRNA. [score:3]
[1 to 20 of 2 sentences]
12
[+] score: 9
Nishimura et al. identified miR-520d-3p as a tumor suppressor upstream of EPHA2, whose expression correlated with favorable outcomes in clinical cohorts [79]. [score:5]
Dual inhibition of EPHA2, using EPHA2 siRNA and nanoliposomes loaded with miR-520d-3p, showed better antitumor efficacy than either monotherapy in vivo. [score:3]
Therapeutic Synergy between miR-520d-3p and EPHA2 siRNA. [score:1]
[1 to 20 of 3 sentences]
13
[+] score: 9
Keklikoglou and colleagues show that overexpression of miR-520/373 members reveals a strong downregulation of transforming growth factor-β (TGF- [β]) signaling and a negative correlation between miR-520c and TGFBR2 expression was observed in estrogen receptor negative (ER(-)) breast cancer patients[20]. [score:8]
The identification of stem cell specific miRNAs(miR-520, miR-302, miR-372, and miR-373) [40, 41], which was predicted to be increased on PAA is an indication that the PAA tissue environment may allow the PNET cells to return to a less differentiated state (S1 Dataset). [score:1]
[1 to 20 of 2 sentences]
14
[+] score: 9
Conversely, mature miR-371, miR-520 and miR-302b (Figure 2B, C) appeared to be expressed in the stem cell populations only (hES and lt-NES), while their corresponding precursors were present both in stem cells and neuronal differentiating cultures. [score:3]
Intriguingly, the maintenance of precursor expression in neuronal cultures for the pluripotency -associated miR-371 and miR-520, as well as for miR-302 might indicate that these miRNAs have further functional roles beyond the switch from self-renewal to differentiation. [score:3]
Among the miRNAs expressed only in hES cells (Group 3), we found miR-371 and miR-520 (Figure 2C), which are known to be associated with pluripotency [29]– [31]. [score:3]
[1 to 20 of 3 sentences]
15
[+] score: 9
The elucidation of the coordinated activity of miR-17-92 and miR-520 miRNAs, as well as of the regulatory networks that they are able to establish with their target genes, can largely contribute to i) the understanding of the physiology of hES cells development and differentiation and to ii) the exploitation of their potential as best candidate resources for both cell replacement therapy and development research. [score:6]
What is of more interest is that these biclusters group together miR-17-92 gene cluster members with those belonging to another important miRNA gene cluster, i. e. miR-520. [score:1]
The association of miR-17-92 with miR-520 was not detected either in mirDIP-A or in biclusters extracted from miRTarBase. [score:1]
Above all, HOCCLUS2 was able to group together, at high levels of the hierarchy, members of the miR-17-92 gene cluster with those belonging to the miR-520 gene cluster. [score:1]
[1 to 20 of 4 sentences]
16
[+] score: 8
On the other hand, miR-515-5p, miR-519c-3p, miR-520d-5p miR-548a-3p, and miR-548c-3p, specifically expressed in oocyte, are not found incorporated in exosome vesicles. [score:3]
Interestingly, we found miR-515-5p, miR-519c-3p, miR-520d-5p, miR-548a-3p, and miR-548c-3p specifically expressed in oocytes, and according to ExoCarta, these have not been found incorporated in exosome vesicles. [score:3]
Moreover, miR-515-5p, miR-519c-3p and miR-520d-5p, members of C19MC, which is a primate-specific cluster, seem to have a role in early embryo development during maternal-zygotic transition, when zygotic transcription starts and maternal mRNAs are degraded (Donker et al., 2012; Battaglia et al., 2016). [score:2]
[1 to 20 of 3 sentences]
17
[+] score: 7
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-23a, hsa-mir-30a, hsa-mir-92a-1, hsa-mir-92a-2, hsa-mir-103a-2, hsa-mir-103a-1, hsa-mir-196a-1, hsa-mir-148a, hsa-mir-30c-2, hsa-mir-30d, hsa-mir-181a-2, hsa-mir-181b-1, hsa-mir-181c, hsa-mir-196a-2, hsa-mir-210, hsa-mir-181a-1, hsa-mir-218-1, hsa-let-7g, hsa-let-7i, hsa-mir-23b, hsa-mir-30b, hsa-mir-128-1, hsa-mir-145, hsa-mir-191, hsa-mir-181b-2, hsa-mir-128-2, hsa-mir-30c-1, hsa-mir-99b, hsa-mir-296, hsa-mir-30e, hsa-mir-361, hsa-mir-337, hsa-mir-148b, hsa-mir-196b, hsa-mir-425, hsa-mir-20b, hsa-mir-486-1, hsa-mir-488, hsa-mir-181d, hsa-mir-498, hsa-mir-519c, hsa-mir-520a, hsa-mir-526b, hsa-mir-506, hsa-mir-92b, hsa-mir-608, hsa-mir-617, hsa-mir-625, hsa-mir-641, hsa-mir-1264, hsa-mir-1271, bta-let-7f-2, bta-mir-103-1, bta-mir-148a, bta-mir-21, bta-mir-30d, bta-mir-128-1, bta-mir-145, bta-mir-181a-2, bta-mir-30b, bta-mir-181b-2, bta-mir-20b, bta-mir-30e, bta-mir-92a-2, bta-let-7d, bta-mir-148b, bta-mir-181c, bta-mir-191, bta-mir-210, bta-mir-23a, bta-mir-361, bta-mir-425, bta-let-7g, bta-mir-30a, bta-let-7a-1, bta-let-7f-1, bta-mir-30c, bta-let-7i, bta-mir-23b, bta-let-7a-2, bta-let-7a-3, bta-let-7b, bta-let-7c, bta-let-7e, bta-mir-103-2, bta-mir-99b, hsa-mir-890, hsa-mir-888, hsa-mir-889, hsa-mir-938, hsa-mir-1184-1, hsa-mir-1203, hsa-mir-1204, hsa-mir-1265, hsa-mir-103b-1, hsa-mir-103b-2, bta-mir-128-2, bta-mir-181d, bta-mir-196a-2, bta-mir-196a-1, bta-mir-196b, bta-mir-218-1, bta-mir-296, bta-mir-30f, bta-mir-486, bta-mir-488, bta-mir-92a-1, bta-mir-92b, bta-mir-1271, bta-mir-181a-1, bta-mir-181b-1, bta-mir-148c, hsa-mir-1184-2, hsa-mir-1184-3, hsa-mir-486-2, bta-mir-1264, bta-mir-148d
Moreover, miR-361-5p, miR-1184 and miR-218-1* were the top among the upregulated miRNAs while miR-1265, miR-20b*, miR-520d-5p and miR-506 were the top among the downregulated miRNAs in the SE animals. [score:7]
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18
[+] score: 7
Akin to the cell lines semi-quantitative revealed an upregulation of 3 miRNAs and again, as further example of that cluster, results were supplemented with qRT-PCR analyses for miR-520. [score:4]
We have shown that all thyroid adenomas with 19q13 rearrangements express significantly higher levels (p≤0.003133) of miR-520 than samples without 19q13 rearrangements (adenomas and surrounding thyroid tissue; for details see Table 1) (Figure 3b). [score:3]
[1 to 20 of 2 sentences]
19
[+] score: 6
In fact, as judged by microarray results at 48 h. p. i., miRNA expression was only modestly modulated (less than 3-fold changes), with most of miRNA resulting slightly downregulated (2.2 fold for miR-181d, miR-302c, miR-372, miR-520e and miR-875; 2.4 fold for miR-520d). [score:6]
[1 to 20 of 1 sentences]
20
[+] score: 6
Here, two miRNAs are associated with Alzheimer’s Disease i. e., hsa-miR-19b and hsa-miR-520d-5p. [score:3]
Following that, miR-19b, miR-19a, miR-520d-5p, miR-524-5p, miR-519b-5p, miR-519a, miR-519c-3p, miR-495, miR-944 and miR-664 regulate 121, 119, 130, 130, 109, 109, 109, 102, 138, 123 genes, respectively. [score:2]
, miR-19b, miR-19a, miR-520d-5p, miR-519b-5p, miR-519a, miR-519c-3p, miR-944 and miR-664) are partially known (i. e., known to only human, but still unknown to rhesus). [score:1]
[1 to 20 of 3 sentences]
21
[+] score: 6
The existing literature implicated hsa-miR-520 h as an important target of ABCG2. [score:3]
Wang and colleagues observed that it resulted in inhibition of cell migration and invasion and decreasing rate of side population cells through transfection of hsa-miR-520 h into Panc-1 cells [30]. [score:3]
[1 to 20 of 2 sentences]
22
[+] score: 6
The authors used a siRNA against the EphA2 oncogene in a preclinical mo del of ovarian cancer and boosted the antitumour effects by addition of miR-520-3d, which synergistically inhibited the EphA2 expression in cancer cells. [score:5]
Nishimura et al. used 1,2-dioleoyl-sn-glycero-3-phosphatidylcholine nanoliposomes loaded with miR-520d-3p and EphA2 siRNA and clearly demonstrated a synergy of this combined treatment to shrink the tumours, which might have broad implications for innovative gene-silencing therapies in clinical trials (Nishimura et al, 2013). [score:1]
[1 to 20 of 2 sentences]
23
[+] score: 6
Five miRNAs (hsa-miR-130a*, hsa-miR-296-5p, hsa-miR-493*, hsa-miR-520d-3p, hsa-miR-661) had different expression levels between latent TB and healthy controls; all of them except hsa-miR-296-5p were up-regulated in healthy controls. [score:6]
[1 to 20 of 1 sentences]
24
[+] score: 6
miR-520 in hepatocellular carcinoma (HCC) cellsThe expression levels of miR-520e were decreased dramatically in HCC cells and clinical HCC tissues resulting from DNA hypermethylation in the upstream region of miR-520e locus, whereas silencing of the expression of miR-520e promoted cell proliferation [50]. [score:5]
miR-520 in hepatocellular carcinoma (HCC) cells. [score:1]
[1 to 20 of 2 sentences]
25
[+] score: 6
Additionally, it was reported that hsa-miR-520 h downregulates ABCG2 in pancreatic cancer cells leading to inhibition of migration, invasion, and side population cells [19]. [score:6]
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26
[+] score: 5
In addition, recent studies have reported that the miR-520 cluster, which is overexpressed in human ES cells, also acts as a tumor suppressor, and that introduction of miR-520h mimics into pancreatic cancer cells results in reduction of side population cells. [score:5]
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27
[+] score: 5
For example, the nerve growth factor receptor pathway was enriched in miR-regulated PINs of miR-520d-3p, miR-497-5p, miR-125a-5p, miR-125b-5p, and miR-31-5p, and the epidermal growth factor receptor pathway was enriched in miR-regulated PINs of miR-520d-3p, miR-21-5p, and miR-497-5p. [score:3]
MIMAT0002856(hsa-miR-520d-3p) GO term GenesAdj. [score:1]
We noted that 7 miRNAs had enriched GO terms related to apoptosis, cell death, and cell proliferation, i. e., miR-520d-3p, miR-497-5p, miR-125b-5p, miR-21-5p, miR-31-5p, let-7c, and miR-125-5p. [score:1]
[1 to 20 of 3 sentences]
28
[+] score: 5
By performing computational target prediction, luciferase reporter system, and mutagenesis assays; five candidate miRNAs (miR-101, miR-520d-5p, miR-140-5p, miR-448 and miR-485-5p) were found to directly target TAL1. [score:5]
[1 to 20 of 1 sentences]
29
[+] score: 5
let-7g-5p, miR-142-3p, miR-16-5p and miR-223-3p were expressed at high levels in all 5 lineages, while miR-134, miR-517c-3p/519a-3p, miR-518d-3p, miR-520d-5p/518a-5p/527 and miR-562 were expressed at low levels in all 5 lineages (Table S5B). [score:5]
[1 to 20 of 1 sentences]
30
[+] score: 5
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-18a, hsa-mir-20a, hsa-mir-21, hsa-mir-22, hsa-mir-23a, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-25, hsa-mir-27a, hsa-mir-29a, hsa-mir-30a, hsa-mir-92a-1, hsa-mir-92a-2, hsa-mir-93, hsa-mir-101-1, hsa-mir-106a, hsa-mir-107, hsa-mir-16-2, hsa-mir-192, hsa-mir-196a-1, hsa-mir-199a-1, hsa-mir-129-1, hsa-mir-148a, hsa-mir-10b, hsa-mir-34a, hsa-mir-181b-1, hsa-mir-181c, hsa-mir-196a-2, hsa-mir-199a-2, hsa-mir-203a, hsa-mir-210, hsa-mir-212, hsa-mir-214, hsa-mir-215, hsa-mir-217, hsa-mir-218-1, hsa-mir-218-2, hsa-mir-221, hsa-mir-222, hsa-mir-223, hsa-mir-200b, hsa-let-7g, hsa-let-7i, hsa-mir-1-2, hsa-mir-15b, hsa-mir-27b, hsa-mir-122, hsa-mir-124-1, hsa-mir-124-2, hsa-mir-124-3, hsa-mir-125b-1, hsa-mir-130a, hsa-mir-141, hsa-mir-142, hsa-mir-143, hsa-mir-145, 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-129-2, hsa-mir-146a, hsa-mir-150, hsa-mir-185, hsa-mir-195, hsa-mir-206, hsa-mir-200c, hsa-mir-1-1, hsa-mir-155, hsa-mir-181b-2, hsa-mir-106b, hsa-mir-29c, hsa-mir-200a, hsa-mir-101-2, hsa-mir-34b, hsa-mir-34c, hsa-mir-130b, hsa-mir-376c, hsa-mir-375, hsa-mir-378a, hsa-mir-148b, hsa-mir-338, hsa-mir-335, hsa-mir-423, hsa-mir-20b, hsa-mir-429, hsa-mir-449a, hsa-mir-433, hsa-mir-451a, hsa-mir-193b, hsa-mir-503, hsa-mir-92b, hsa-mir-610, hsa-mir-630, hsa-mir-650, hsa-mir-449b, hsa-mir-421, hsa-mir-449c, hsa-mir-378d-2, hsa-mir-744, hsa-mir-1207, hsa-mir-1266, hsa-mir-378b, hsa-mir-378c, hsa-mir-378d-1, hsa-mir-378e, hsa-mir-378f, hsa-mir-378g, hsa-mir-378h, hsa-mir-4512, hsa-mir-378i, hsa-mir-203b, hsa-mir-451b, hsa-mir-378j
Moreover, GC patients with over -expression of miR-107 [28, 29, 30], miR-143 [40], miR-145 [41, 42], miR-181b/c [17, 47, 48, 55, 56], miR-196a/b [59], miR-20b [23, 66], miR-23a/b [77, 78, 79], miR-34 [17, 47, 48, 55, 56] and miR-630 [100] and decreased expression of miR-1 [111], miR-1207-5p [121], miR-125a-3p/-5p [24, 125, 126, 127], miR-185 [140], miR-193b [60], miR-20a [111], miR-206 [150, 151], miR-215 [142], miR-217 [153], miR-27a [111], miR-29c [169], miR-34a [172, 173], miR-423-5p [111], and miR-520d-3p [99] indicate advanced tumor stage or TNM stage. [score:5]
[1 to 20 of 1 sentences]
31
[+] score: 4
The tumor suppressor p21, regulating transition through the cell cycle and acting downstream of p53, has already been associated with hsa-miR520 belonging to the miR-106/302 family [14]. [score:4]
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32
[+] score: 4
Indicated are select oncomiRs from the miR-17-92 and miR-106b-25 clusters and miR-520/373 family, which all have enriched putative target sites in Ago1-bound sequences. [score:3]
Interestingly, approximately one third of the 49 miRNAs are known oncomiRs including those from the miR-17-92 and miR-106b-25 clusters, as well as the miR-520/373 family (Figure 6B, Table S9). [score:1]
[1 to 20 of 2 sentences]
33
[+] score: 4
[37] George Calin and his colleagues reported that dual targeting of EphA2 using siRNA-EphA2 and miR-520d-3p exhibits synergistic inhibition of EphA2 and significantly augments tumor regression compared to either monotherapy alone both in vitro and in vivo. [score:4]
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34
[+] score: 4
The mir-520 group suppresses NFκB and TGF-β signaling, again in the context of cancerous cells [27], but given the roles of both signaling molecules in cytokine signaling and regulation, it is likely that this microRNA has alternative functions in these ILCs. [score:4]
[1 to 20 of 1 sentences]
35
[+] score: 4
For example, we found that miR-520d*/miR-661 co-down-regulate EGFR and KRAS. [score:4]
[1 to 20 of 1 sentences]
36
[+] score: 3
The miRNA-520 cluster on chromosome 19 was highly expressed in undifferentiated hESCs, and might be closely involved in hESC function [156, 166]. [score:3]
[1 to 20 of 1 sentences]
37
[+] score: 3
Then, we artificially altered the expression level of miR-520-3p by HOXA-AS2, si-HOXA-AS2, miR-520c-3p or antisense miR-520c-3p (Anti-520-3p) in breast cancer cells, and qRT-PCR was used to validate the transfection efficiency (P < 0.05, Figure 6C, 6D). [score:3]
[1 to 20 of 1 sentences]
38
[+] score: 3
Indeed, we found that the levels of three placental microRNAs (hsa-miR-526a, hsa-miR-527 and hsa-miR-520d-5p) could be used to accurately distinguish pregnant from non pregnant women (Figure 5). [score:1]
The y axis indicates the amount of mir-527, and the x axis indicates the average level of miR-520d-5p and miR-526a. [score:1]
A) The three placental microRNAs (miR-527, miR-520d-5p and miR-526a) are highly abundant in the sera of pregnant women and their levels rise as pregnancy progresses. [score:1]
[1 to 20 of 3 sentences]
39
[+] score: 3
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-mir-16-1, hsa-mir-17, hsa-mir-18a, hsa-mir-19b-1, hsa-mir-19b-2, hsa-mir-20a, hsa-mir-21, hsa-mir-26a-1, hsa-mir-26b, hsa-mir-29a, hsa-mir-31, hsa-mir-99a, hsa-mir-100, hsa-mir-29b-1, hsa-mir-29b-2, hsa-mir-106a, hsa-mir-16-2, hsa-mir-192, hsa-mir-199a-1, hsa-mir-208a, hsa-mir-30c-2, hsa-mir-147a, hsa-mir-10a, hsa-mir-34a, hsa-mir-181b-1, hsa-mir-199a-2, hsa-mir-203a, hsa-mir-204, hsa-mir-217, hsa-mir-219a-1, hsa-mir-221, hsa-mir-222, hsa-mir-223, hsa-mir-200b, hsa-mir-27b, hsa-mir-30b, hsa-mir-122, hsa-mir-125b-1, hsa-mir-132, hsa-mir-140, hsa-mir-142, hsa-mir-143, hsa-mir-145, hsa-mir-125a, hsa-mir-125b-2, hsa-mir-126, hsa-mir-146a, hsa-mir-150, hsa-mir-185, hsa-mir-193a, hsa-mir-195, hsa-mir-200c, hsa-mir-155, hsa-mir-181b-2, hsa-mir-30c-1, hsa-mir-219a-2, hsa-mir-296, hsa-mir-130b, hsa-mir-30e, hsa-mir-26a-2, hsa-mir-302d, hsa-mir-374a, hsa-mir-375, hsa-mir-378a, hsa-mir-330, hsa-mir-328, hsa-mir-342, hsa-mir-325, hsa-mir-424, hsa-mir-429, hsa-mir-450a-1, hsa-mir-486-1, hsa-mir-146b, hsa-mir-497, hsa-mir-520e, hsa-mir-520f, hsa-mir-520a, hsa-mir-520b, hsa-mir-520c, hsa-mir-520g, hsa-mir-520h, hsa-mir-450a-2, hsa-mir-503, hsa-mir-608, hsa-mir-625, hsa-mir-629, hsa-mir-663a, hsa-mir-1271, hsa-mir-769, hsa-mir-378d-2, hsa-mir-675, hsa-mir-147b, hsa-mir-374b, hsa-mir-663b, hsa-mir-378b, hsa-mir-378c, hsa-mir-374c, hsa-mir-378d-1, hsa-mir-378e, hsa-mir-378f, hsa-mir-378g, hsa-mir-378h, hsa-mir-378i, hsa-mir-4661, hsa-mir-219b, hsa-mir-203b, hsa-mir-378j, hsa-mir-486-2
In HepG2 cells, EGCG differentially represses the expression of five miRNAs (miR-30b*, miR-453, miR-520-e, miR-629, and miR-608) involved in inflammatory pathways, the peroxisome proliferators-activated receptors (PPAR) signaling pathway, the insulin signaling pathway, glycolysis and gluconeogenesis, oxidative phosphorylation, and glutathione metabolism [127]. [score:3]
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40
[+] score: 3
Moreover, compared with the healthy gingiva, in periodontitis cases, six miRNAs (let-7a, let-7c, miR-130a, miR-301a, miR-520d and miR-548a) were up-regulated more than eightfold [25]. [score:3]
[1 to 20 of 1 sentences]
41
[+] score: 3
Several miRNA families, including the human (hsa)-miR-302, hsa-miR-106, hsa-miR-372, hsa-miR-17, hsa-miR-520, hsa-miR-195 and hsa-miR-200 families [155] were up-regulated specifically in hPSCs compared to mature differentiated cell types. [score:3]
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42
[+] score: 2
More recently, miR-520d-3p mimetic was found to synergize with EphA2 siRNA to reduce ovarian tumor size and invasive capacity (Nishimura et al. 2013). [score:1]
Interestingly, miR-520d-3p with EphA2 is an independent prognostic marker for serous ovarian cancer (Nishimura et al. 2013). [score:1]
[1 to 20 of 2 sentences]
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Therefore, when we discuss the functions of miR-373 here, we should bear in mind that other members of miR-520/373 family may possess the same functions. [score:1]
miR-373 is one member of miR520/373 family, which consists of three different miRNA clusters possessing identical seed region, miR-302/367, miR-371/372/373 and miR-520 [8, 18, 22]. [score:1]
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miRNA ΔΔCT(mean) p-value miR-374 -0.4458 0.454 miR-142-3p -0.4136 0.4322 miR-523 -0.5518 0.3424 miR-374-5p -0.2611 0.6425 miR-376c -0.4312 0.5867 miR-27a -0.3863 0.4776 miR-520d-5p -0.3081 0.7506 miR-122 -0.0856 0.9251 miR-485-3p -0.2611 0.6392 miR-21 -0.3976 0.5261 miR-218 -1.332 0.1659 miR-374 -0.4458 0.454 Comparison of mean ΔΔCT’s for various plasma miRNA from plasma samples drawn from the same 7 individuals on the same day 12 hours apart. [score:1]
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miR-373 belongs to the miR-520/-373 family, which consists of three different miRNA clusters (miR-302/-367, miR-371/-372/-373, and miR-520) [27]. [score:1]
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miR-372, miR-373, miR-302, miR-520 and some other miRNAs are members of miR-93 family. [score:1]
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Other miRNAs from this paper: hsa-mir-29a, hsa-mir-101-1, hsa-mir-139, hsa-mir-218-1, hsa-mir-218-2, hsa-mir-142, hsa-mir-144, hsa-mir-127, hsa-mir-154, hsa-mir-185, hsa-mir-195, hsa-mir-29c, hsa-mir-101-2, hsa-mir-380, hsa-mir-381, hsa-mir-323a, hsa-mir-520e, hsa-mir-520a, hsa-mir-518c, hsa-mir-518a-1, hsa-mir-518d, hsa-mir-518a-2, hsa-mir-519a-1, hsa-mir-519a-2, hsa-mir-513a-1, hsa-mir-513a-2, hsa-mir-509-1, hsa-mir-576, hsa-mir-548a-1, hsa-mir-586, hsa-mir-548b, hsa-mir-548a-2, hsa-mir-599, hsa-mir-548a-3, hsa-mir-607, hsa-mir-613, hsa-mir-548c, hsa-mir-625, hsa-mir-634, hsa-mir-642a, hsa-mir-548d-1, hsa-mir-548d-2, hsa-mir-656, hsa-mir-509-2, hsa-mir-509-3, hsa-mir-1208, hsa-mir-548e, hsa-mir-548j, hsa-mir-1290, hsa-mir-548k, hsa-mir-548l, hsa-mir-548f-1, hsa-mir-548f-2, hsa-mir-548f-3, hsa-mir-548f-4, hsa-mir-548f-5, hsa-mir-1247, hsa-mir-548g, hsa-mir-548n, hsa-mir-548m, hsa-mir-548o, 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-1324, hsa-mir-1825, hsa-mir-548q, hsa-mir-548s, hsa-mir-548t, hsa-mir-548u, hsa-mir-548v, hsa-mir-323b, hsa-mir-548w, hsa-mir-548x, hsa-mir-548y, hsa-mir-642b, hsa-mir-548z, hsa-mir-548aa-1, hsa-mir-548aa-2, hsa-mir-548o-2, hsa-mir-548h-5, hsa-mir-548ab, 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-548ai, hsa-mir-548aj-1, hsa-mir-548aj-2, hsa-mir-548x-2, hsa-mir-548ak, hsa-mir-548al, hsa-mir-548am, hsa-mir-548an, hsa-mir-548ao, hsa-mir-548ap, 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-548ay, hsa-mir-548az, hsa-mir-548ba, hsa-mir-548bb, hsa-mir-548bc
Seven miRNAs are included in the C19MC cluster, which is a primate-specific cluster on chromosome 19 (miR-518a-5p, miR-518c, miR-518d-3p, miR-519a, miR-520a-5p, miR-520d-3p, miR-520e). [score:1]
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We observed focal areas of hypomethylation of miR-520 and 5′ from the coding sequence in lymphomas, which may represent a permissive state for the binding of putative transcriptional repressors. [score:1]
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Using stepwise artificial neural networks (ANN) analysis, Lowery et al. identified a predictive miRNA signature (miR-520d, miR-181c, miR-302c, miR-376b, miR-30e) corresponding with Her2/neureceptor status [30]. [score:1]
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By comparison, miRNA transcripts of the C19MC cluster (miR-512, miR-516b, miR-520, and miR-525) were unchanged (Fig. 5). [score:1]
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We can see that, while bicluster Z' associates MUC17 with miR-17, miR-20a and miR-20b (Figure 9(a)), biclusters at levels 3 and 4 (Figures 9(b) and 9(c)) also include other miRNAs, some belonging to the miR-17-92 gene cluster and others to the miR-520 gene cluster. [score:1]
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For example, circulating miRNAs were found in the sera of pregnant women [27]: miRNA-526a, miRNA-527 and miRNA-520d-5p showed a considerably high fold-change and could be used to distinguish pregnant from non-pregnant women with high accuracy. [score:1]
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Interestingly, except for isomiR of hsa-miR-520 g, other isomiRs with 3′ additions had the same 5′ ends and “seed sequences” with their canonical miRNA sequences in the miRBase database. [score:1]
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Thus, in breast cancer, which represents the most common malignancy among women in the world, miRNAs such as miR-9, miR-10b, miR-21, miR-103/107, miR-132, miR-373, and miR-520 stimulate metastasis, while miR-7, miR-30, miR-31, miR-126, miR-145, miR-146, miR-200, miR-205, miR-335, miR-661, and miRNAs of the let-7 families in contrast impair the different steps of metastatic process, from epithelial-to-mesenchymal transition to local invasion to colonisation and angiogenesis [61]. [score:1]
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