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16 publications mentioning hsa-mir-522

Open access articles that are associated with the species Homo sapiens and mention the gene name mir-522. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

[+] score: 262
Subsequently, we examined the DENND2D expression level in tumor tissues and their matched normal tissues and found that DENND2D was downregulated at the mRNA level, whereas miR-522 was upregulated in tumor tissues. [score:9]
How to cite this article: Zhang, T. et al. Downregulation of miR-522 suppresses proliferation and metastasis of non-small cell lung cancer cells by directly targeting DENN/MADD domain containing 2D. [score:9]
The specific overexpression of miR-522 significantly downregulated the DENND2D protein level (Fig. 7a), whereas the suppression of miR-522 increased the DENND2D protein level (Fig. 7b). [score:8]
However, ectopic miR-522 expression decreased DENND2D only at the protein level and not at the mRNA level, indicating that it did not degrade but, rather, inhibited DENND2D mRNA translation. [score:7]
These miRNAs have been demonstrated to target genes that play important roles in lung carcinogenesis and have emerged as biomarkers for tumor diagnosis, prognosis and prediction of responses to treatment 16. miR-522 is a member of the chromosome 19 miRNA cluster (C19MC), a 100-kb, primate-restricted region that encodes 54 tandem miRNAs; this cluster is the largest miRNA cluster in the human genome 17. miR-522 is reportedly upregulated in HCC and may contribute to tumor development 18 19. [score:7]
As a consequence, the pathological loss of miR-522 may suppress tumorigenesis by directly regulating the tumor suppressor gene DENND2D. [score:7]
The overexpression of miR-522 in A549 and H460 cells was sufficient to suppress the expression of DENND2D. [score:7]
As shown in Fig. 2b, the overexpression of miR-522 significantly increased the viability of A549 and H460 cells compared with their corresponding controls in different time points, whereas miR-522 inhibitor suppressed cell viability in both cell lines. [score:6]
Because miR-522 expression was upregulated in NSCLC tissues and cells, we identified the functional roles of miR-522 in all aspects of NSCLC progression, including cell proliferation, apoptosis, migration and invasion. [score:6]
Figure 4a,b show that overexpression of miR-522 markedly promoted the mobility of A549 and H460 cells compared with the control group, whereas miR-522 inhibitor suppressed cell migration. [score:6]
The expression of miR-522 was significantly upregulated in NSCLC tissues and cell lines. [score:6]
DENND2D, a tumor suppressor gene in several cancers, was identified as a direct and functional target of miR-522, as shown in Fig. 6a. [score:6]
From result showed in Fig. 8, we demonstrated that miR-mask designed to be fully complementary to the target DENND2D sequence of miR-522 reversed the effects of miR-522 on NSCLC cell proliferation and metastasis, indicating that miR-522 may function as an oncogene in NSCLC cells by directly targeting DENND2D. [score:6]
miR-522 inhibitor suppresses cell proliferation and induces apoptosis in NSCLC cells. [score:5]
The upregulation of miR-522 is associated with the development of glioblastoma and increased tumor cell proliferation in vitro 20. [score:5]
We first either overexpressed or inhibited miR-522 in A549 and H460 cells. [score:5]
To explore the molecular mechanisms by which miR-522 executes its function, we used several bioinformatic predictions, such as TargetScan and miRanda, to determine the potential target of miR-522. [score:5]
Data are presented as the mean ± S. E. M. (a) Cells were transfected with miR-522 or miR-522 inhibitor, and the expression of miR-522 was analyzed by qRT-PCR. [score:5]
We also focus on the molecular mechanisms by which DENND2D, one of the direct targets of miR-522, may contribute to NSCLC development. [score:5]
To clarify the underlying molecular mechanisms by which miR-522 participates in NSCLC progression, we used ten different types of prediction software to predict gene targets for miR-522, which identified DENND2D as a potential downstream target. [score:5]
miR-522 may function as an oncogene by directly targeting DENND2D to regulate NSCLC. [score:5]
We confirmed that co-transfection of miR-522 and miR-mask acted against the overexpression of miR-522 -induced NSCLC cell proliferation, and transfection of miR-mask alone suppressed the effect of endogenous miR-522 (Fig. 8a,b; Supplemental Fig. 4a & 4b). [score:5]
Overexpression of miR-522 dramatically increased the migration and invasiveness of NSCLC cells, whereas miR-522 inhibition reversed these effects. [score:5]
In addition, miR-522 was dramatically upregulated in all 4 lung cancer cell lines, i. e., A549, H460, PG-BE1 and H358 (Fig. 1b). [score:4]
Moreover, the fact that miR-522 was also found upregulated in human NSCLC tissues as in the cell lines is suggestive of the potential role of this miRNA in the tumorigenesis. [score:4]
We then used a relative luciferase reporter assay with the DENND2D 3′-untranslated region (3′UTR) to demonstrate that miR-522 dramatically inhibited the luciferase activity of the wild-type (WT) 3’UTR but not that of the mutant (Mut) 3’ UTR of DENND2D (Fig. 6b,c). [score:4]
miR-522 negatively regulates DENND2D expression. [score:4]
miR-522 was significantly upregulated, indicating that miR-522 may play an important role in NSCLC carcinogenesis and progression. [score:4]
The cells were starved in serum-free medium for 24 h, and then transiently transfected with miR-522 mimics, miR-522 inhibitors or negative controls, and miR-mask (RiboBio Co. [score:3]
To better understand the role of miR-522 in NSCLC, we first analyzed the effect of miR-522 expression on the tissues of NSCLC patients and four NSCLC cell lines. [score:3]
A549 and H460 cells were transfected with miR-522 or miR-522 inhibitor for 24 h, 48 h, and 72 h. All independent experiments were performed 3 times. [score:3]
miR-522 is highly expressed in NSCLC tissues and cell lines. [score:3]
These findings are particularly interesting because our data show that the inhibition of miR-522 effectively induced apoptosis in A549 and H460 cells. [score:3]
Furthermore, miR-522 has been shown to enhance the ability of triple -negative breast cancer cells to survive detachment, invade through a membrane, and express mesenchymal genes, properties that are associated with metastasis 17. [score:3]
Identification of DENND2D as a miR-522 target gene. [score:3]
To study the expression and significance of miR-522 in NSCLC carcinogenesis, we measured the expression of miR-522 in 37 pairs of NSCLC tissues and their matched normal lung tissues using qRT-PCR. [score:3]
The mechanism by which miR-522 affects NSCLC cells was associated with changes in the expression of DENND2D. [score:3]
The overexpression of miR-522 effectively increased NSCLC cell migration and invasion, whereas miR-mask reversed the effects of miR-522 (Fig. 8c,d; Supplemental Fig. 4c & 4d). [score:3]
The expression of miR-522 was higher in A549 and H460 cells than in the other two cell lines. [score:3]
Furthermore, a previous study showed that miR-522 induces G1 cell-cycle arrest and causes cells to detach without anoikis, become invasive, and express mesenchymal genes 17. [score:3]
The inhibition of miR-522 effectively decreased proliferation and induced apoptosis in NSCLC cells. [score:3]
293T cells (2 × 10 [4] cells/well) were cultivated in a 24-well plate and co -transfected with miR-522 mimics or miR-522 inhibitors and plasmid using Lipofectamine 2000 reagent. [score:3]
miR-522 was significantly upregulated in NSCLC tissues compared with their matched normal tissues (Fig. 1a). [score:3]
Relationship between miR-522 expression and clinicopathological parameters in 37 fresh samples of lung cancers. [score:3]
An was used according to the manufacturer’s instructions to detect apoptosis following treatment with miR-522 or miR-522 inhibitor (Beyotime, Shanghai, China). [score:3]
In our study, the miR-mask was designed to be fully complementary to the target DENND2D sequence of miR-522. [score:3]
miR-522 expression in NSCLC tissues and cell lines by qRT-PCR. [score:3]
The transfection of miR-522 inhibitor dramatically increased the apoptosis rate, whereas co-transfection of miR-522 attenuated these beneficial effects (Fig. 3). [score:3]
Furthermore, the overexpression of miR-522 dramatically increased the ability of NSCLC cells to migrate and invade. [score:3]
miR-522 may therefore represent a novel therapeutically relevant cellular target for the treatment of NSCLC patients. [score:3]
The expression of miR-522 negatively correlates with the DENND2D protein level in NSCLC cell lines. [score:3]
Consistent with a previous study reported by Zhang et al. 20, miR-522 promoted A549 and H460 cell proliferation, an effect that could be reversed by miR-522 inhibitor. [score:3]
Based on the above results, we examined the expression of DENND2D responses to altered levels of miR-522 in vitro. [score:3]
In Fig. 2c, more new proliferative cells double labeled with EdU and Hoechst 33342 were observed under transfection of miR-522 for 24 h compared with miR-control, whereas the number was markedly decreased after transfection of miR-522 inhibitor. [score:2]
To examine whether DENND2D is the key factor that miR-522 regulates proliferation and metastasis in NSCLC cells, we detected the effects of miR-522 with a corresponding miR-mask. [score:2]
Transwell assays with Matrigel were performed to evaluate the ability of cells to invade; exogenously increased miR-522 expression significantly increased the number of invasive cells, whereas miR-522 inhibitor had the opposite effect on NSCLC cells invasion (Fig. 5). [score:2]
DENND2D is involved in miR-522 induced proliferation and metastasis of NSCLC cells. [score:1]
The results for 48 h and 72 h were provided in Supplemental Fig. 2. To evaluate whether miR-522 inhibitor could induce apoptosis, we examined Annexin V-FITC/PI staining by flow cytometry. [score:1]
Effects of miR-522 on human NSCLC cells apoptosis. [score:1]
The levels of miR-522 and DENND2D mRNA were determined using a SYBR Green I incorporation method and an ABI 7500 fast Real Time PCR system (Applied Biosystems, USA). [score:1]
Effects of miR-522 on the proliferation of human NSCLC cells. [score:1]
However, it should be pointed out that our in vitro observations may not be readily applied to in vivo situations in the absence of in vivo studies and the possible role of miR-522 in pathogenesis of lung cancer merits further studies using animal mo dels of tumors. [score:1]
U6 and GAPDH were used as internal controls for miR-522 and DENND2D, respectively 30. [score:1]
In this study, we first describe a potential role for miR-522 in the proliferation and metastasis of NSCLC. [score:1]
To certify that DENND2D is required for miR-522 to mediate its functions, we used a miR-mask technology. [score:1]
A luciferase assay showed that miR-522 directly bound to the 3′-UTR of DENND2D. [score:1]
Based on the above results, we hypothesized a relationship between miR-522 and NSCLC cell proliferation. [score:1]
However, the detailed role of miR-522 in NSCLC remains unknown. [score:1]
Overall, our study is the first to show that miR-522 plays an important role in NSCLC carcinogenesis by affecting cell proliferation, apoptosis, migration and invasion. [score:1]
Nonetheless, like numerous published studies with similar approaches at the cellular level, our findings serve to provide clues for the miR-522 functioning in tumor growth and metastasis of NSCLC. [score:1]
The correlation between miR-522 and DENND2D in NSCLC cells. [score:1]
Effects of miR-522 on the migration of NSCLC cells. [score:1]
DENND2D is involved in miR-522 induced NSCLC proliferation and metastasis. [score:1]
However, transfection of miR-522 alone had no effect on apoptosis in Supplemental Fig. 3. Cancer metastasis is the primary cause of cancer -associated death. [score:1]
In the present study, we reveal a novel role of miR-522 in the proliferation and metastasis of NSCLC cells. [score:1]
miR-522 increases NSCLC cell migration and invasion. [score:1]
Effects of miR-522 on the invasion of NSCLC cells. [score:1]
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[+] score: 80
Other miRNAs from this paper: hsa-mir-519d
If in addition to regulating PLIN4 expression PUFA n3 down-regulates miR-522, we would expect increasing PUFA n3 intake to have a more dramatic effect in reducing weight for subjects carrying the minor allele compared to non-carriers. [score:6]
While there is evidence for miR-522 expression in placenta, testis, thymus, brain and prostate to our knowledge expression has not been demonstrated in adipose tissue [25], [27]. [score:5]
Figure 3a shows the normalized relative expression of miR-522, with highest expression in HepG2 cells, pre-adipocytes and adipocytes. [score:5]
It is likely that miR-522 is important for development given its temporal expression in placenta and fetal tissues, however its role in adipocytes is unknown. [score:4]
Thus to determine if miR-522 is expressed in human adipoctyes, we performed RT-PCR on total RNA samples extracted from cultured COS7, HEK293T, HepG2 cells, and primary human pre-adipocyte and mature adipocytes. [score:3]
Specifically, if the miR-522 PLIN4 interaction is absent in those homozygous for the G allele, reducing miR-522 activity through increasing PUFA n3 will have no additional effect on increasing PLIN4 expression, and therefore no added contribution to weight loss. [score:3]
miR-522 targets the 3′UTR of PLIN4 containing the rs8887 minor A allele. [score:3]
COS7 cells, plated into 12-well plates (Costar), were co -transfected with 1 µg of the pmiR-LucPLIN4-G or pmiR-LucPLIN4-A luciferase reporter vectors and 40 nM mi RIDIAN miR-522 mimic or an equal concentration of a non -targeting control mimic sequence (Dharmacon) using the Lipofectamine 2000 Reagent (Invitrogen). [score:3]
These data indicate an ability of miR-522 to bind and partially repress luciferase expression via the PLIN4 3′UTR segment when carrying the derived A allele of rs8887. [score:3]
In silico analysis of the PLIN4 mRNA sequence predicted the minor A allele of rs8887 generates a novel seed site for miR-522 and our ex vivo luciferase data indicated that miR-522 reduced PLIN4 protein levels 20% via the PLIN4 3′UTR target site created by the rs8887 A allele. [score:3]
It may be miR-522 is dysregulated in the obese and thus contributes to the dysregulation of adipogenic pathways as suggested for another C19MC member, miR-519d [37]. [score:3]
To determine the effect of miR-522 on the PLIN4 3′UTR, we cloned into the siCHECK2 luciferase expression vector a 560-bp region of the PLIN4 3′UTR from genomic DNA of subjects homozygous for either rs8887 allele. [score:3]
A) Relative miR-522 expression across indicated cell types, hek293T (293T), Cos7 (c7), hepG2 (hG2), pre-adpocytes (pre-Ad) and adipocytes(Ad). [score:3]
B) Luciferase expression of pmiR-LucPLIN4-G or A constructs with miR-522 (522) or control mimic (CM). [score:3]
We hypothesize that binding between rs8887 and mir-522 results in suboptimal expression of PLIN4, thereby contributing to the elevation in anthropometrics observed in our association analyses. [score:3]
Identifying the function(s) of miR-522 and the conditions that induce its activation and repression will help clarify its role in mammalian development and as a potential modulator of obesity phenotypes. [score:2]
C19MC is thought to be a product of an AluJ/AluS insertion into chromosome 19 during an early stage of primate evolution suggesting a role for miR-522 in higher development and phenotypic plasticity [26]. [score:2]
The ability of miR-522 to regulate PLIN4 3′UTR was examined. [score:2]
C) Luciferase expression of pmiR-LucPLIN4-A constructs with increasing concentration of miR-522 compared to control mimic. [score:2]
Due to what little is known of PLIN4 regulation, it is difficult to propose a mechanism by which the miR-522 rs8887 interaction together with PUFA n3 could modulate anthropometrics. [score:2]
The miR-522 seed site is highlighted in gray, and the rs8887 variants are in bold. [score:1]
Our phylogenetic analysis indicates that variation at the rs8887 position resulting in the PLIN4 miR-522 MRE is specific to humans and likely undergoing drift. [score:1]
Both programs predicted the binding of miR-522 with perfect complementarity to a seed site in the PLIN4 mRNA when containing the minor A allele (Figure 2 ). [score:1]
miR-522 targets the 3′UTR of PLIN4 containing the rs8887 minor A alleleWe next investigated the functional potential of rs8887. [score:1]
Diagram of the miR-522: PLIN4 3′UTR sequences with the A or G allele. [score:1]
The rs8887 minor A allele creates a novel miR-522 MRE in the PLIN4 3′UTR. [score:1]
0169) or LucPLIN4-G in the presence of mir-522 or control mimic (P = . [score:1]
miR-522 maps within the chromosome 19 microRNA cluster (C19MC), the largest known primate specific microRNA gene cluster [25], [26]. [score:1]
The PLIN4 3′UTR with the A allele creates a miR-522 MRE. [score:1]
Statistical Analysis: P values for the difference between luciferase activity obtained for LucPLIN4-A in the presence of mir-522 or control mimic (P = . [score:1]
We find no evidence for a PLIN4 pseudogene in the human genome which strengthens the implications of the miR-522-PLIN4 interaction we describe here. [score:1]
0017944.g002 Figure 2The rs8887 minor A allele creates a novel miR-522 MRE in the PLIN4 3′UTR. [score:1]
The effect of increasing concentrations of miR-522 on PLIN4 3′UTR with the A allele is saturated at 20 nM of miR-522 (Figure 3c ). [score:1]
0017944.g003 Figure 3The PLIN4 3′UTR with the A allele creates a miR-522 MRE. [score:1]
Alternatively, miR-522 may be modulated by environmental factors which influence PLIN4 through rs8887 as suggested for several other miRs [38]. [score:1]
COS7 cells were co -transfected with miR-522 mimic or control mimic, and with the A allele or the G allele PLIN4 3′UTR vector. [score:1]
Our results indicated the rs8887 SNP creates a miR-522 miR recognition element (MRE) in the PLIN4 3′UTR. [score:1]
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[+] score: 17
The IMPACT-Seq technique was utilized to experimentally demonstrate that miR-522-3p can regulate human endoglin expression and that the MRE for this miRNA was localized to the 5′-UTR region of human endoglin mRNA isoforms (Tan et al., 2014[153]) (Table 7 (Tab. [score:4]
Given that this predicted MRE is harbored in the 5′-UTR region of the human endoglin mRNA isoforms, miR-522-3p/endoglin mRNA interactions would not be identified by the target algorithms discussed above since they are not programmed to analyze this region. [score:3]
Furthermore, with the tendency of miR-522-3p to interact with noncanonical MRE sequences, Tan et al. (2014[153]) demonstrated that of the 2,467 3′-UTR miR-522-3p MREs that they identified only 111 were predicted by target algorithms. [score:3]
7) (References in Table 7: let-7b-5p: Selbach et al., 2008[145]; miR-16-5p: Balakrishnan et al., 2014[14]; miR-20a-3p: Balakrishnan et al., 2014[14]; miR-23b-5p: Balakrishnan et al., 2014[14]; miR-29a-5p: Balakrishnan et al., 2014[14]; miR-103a-3p: Balakrishnan et al., 2014[14]; miR-107: Balakrishnan et al., 2014[14]; miR-532-5p: Haecker et al., 2012[63]; miR-628-5p: Balakrishnan et al., 2014[14]; miR-522-3p: Tan et al., 2014[153]) documents ten human experimentally supported miRNA/endoglin mRNA interactions, and the methodology utilized to substantiate the interaction, the tissue and/or cell line used for experimentation, the location of the MRE if known, the type of interaction (direct or indirect), and the literature reference. [score:3]
In contrast, miR-23b-5p, miR-522-3p, and miR-532-5p (experimentally cataloged miRNAs which target human endoglin mRNAs, Table 7 (Tab. [score:3]
Therefore, the human S-endoglin mRNA was manually screened for the miR-522-3p MRE. [score:1]
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[+] score: 16
The miR-512-3p and miR-522* were up-regulated between the normal cervical tissues and CINI and CINIII samples and had normal expression in cervical carcinoma. [score:6]
For miR-522* we could not find any predictive targets, but the miRNA expression pattern suggests that this miRNA may also play a role in cervical abnormal transformation. [score:5]
Two miRNAs exhibited relative increased expression in the transition from normal cervix to atypical dysplasia and decreased expression in the transition from atypical dysplasia to cervical carcinoma, namely miR-522* and miR-512-3p (Figure 4C). [score:5]
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[+] score: 9
Other miRNAs from this paper: hsa-mir-200a
Zhang T Downregulation of miR-522 suppresses proliferation and metastasis of non-small cell lung cancer cells by directly targeting DENN/MADD domain containing 2DSci. [score:9]
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[+] score: 9
Zhang T Downregulation of miR-522 suppresses proliferation and metastasis of non-small cell lung cancer cells by directly targeting DENN/MADD domain containing 2DSci. [score:9]
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[+] score: 8
RT-qPCR was performed to evaluate the expression levels of hsa_circ_0043497 (A) and its top 5 predicted miRNA targets (miR-335-3p, miR-186-5p, miR-380-5p, miR-296-3p and miR-522-3p) (B), hsa_circ_0001204 (C) and its top 5 predicted miRNA targets (miR-612, miR-657, miR-362-3p, miR-377-3p and miR-136-5p) (D) in ten human MDMs after 24 h of infection with H37Rv. [score:5]
The potential miRNAs targets of hsa_circ_0043497 include miR-335-3p, miR-186-5p, miR-380-5p, miR-296-3p and miR-522-3p. [score:3]
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[+] score: 8
In addition, 10 miRNAs; miR-720, miR-891a, miR-522, miR-518c, miR-3665, miR-3620, miR-382, miR-452, miR-122 and miR-147 were found down-regulated in the patient group, indicating tumor suppressor properties. [score:6]
Finally, ten miRNAs were found overexpressed in the control group when compared to the patients group (relapsed or in Complete Remission (CR)); miR-720 (I), miR-891a (J), miR-522 (K), miR-518c (L), miR-3665 (M), miR-891a (N), miR-382 (O), miR-452 (P), miR-122 (Q), miR-147 (R). [score:2]
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[+] score: 7
miR-522, miR-139-3p, miR-520c-5p, miR-518d-5p, miR-146b-5p, miR-34a, miR-526a, miR-193a-3p, miR-221, miR-4674 were significantly upregulated and miR-760 was downregulated in ECSCs (Figure 2A). [score:7]
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[+] score: 6
none —[51] antropometrics (obesity related phenotype) miR-522 PLIN4 rs8887 G>A (A creates a new binding site) in vitro: luciferase expression vectors in COS7 cells (with miR mimic or control). [score:3]
This study reported that PLIN4 is regulated by miR-522 only in the rs8887A variant. [score:2]
PLIN4 | miR-522. [score:1]
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[+] score: 6
In NTera-2 cells, this cluster is expressed, but only two of its miRNAs (miR-517c and miR-522) were downregulated. [score:6]
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[+] score: 5
These findings are consistent with a recent report in which miR-522 expression induce cell motility by targeting DENND2D in lung cancer 40. [score:5]
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[+] score: 4
Indeed, some miRNAs that have been previously linked to carcinogenesis of different organs and tissues, such as miR-424-5p (previous ID: miR-424), miR-221-5p (previous ID: miR-221*), miR-675, miR-647, miR-125a-5p, miR-214-3p (previous ID: miR-214), miR-130b-3p (previous ID: miR-130b), miR-522-3p (previous ID: miR-522), and miR-16-5p (previous ID: miR-16) [18- 21] were found to be up- or downregulated in our analysis. [score:4]
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[+] score: 4
Tan SM, Kirchner R, Jin J, Hofmann O, McReynolds L, Hide W, Lieberman J. Sequencing of captive target transcripts identifies the network of regulated genes and functions of primate-specific miR-522. [score:4]
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[+] score: 2
The miR-522 binding site with A allele was not found in Neanderthal and non-human primates suggesting a recent evolutionally change. [score:1]
The study by Richardson et al. revealed that the PLIN4 3’ UTR has undergone nucleotide substitution allowing the binding of miR-522 for human individuals with A but not G allele. [score:1]
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[+] score: 1
For the miRNA-Seq data sets, the following MIMAT numbers were analysed: MIMAT0000259 (hsa-miR-182-5p), MIMAT0000222 (hsa-miR-192-5p), MIMAT0002868 (hsa-miR-522-3p), MIMAT0018937 (hsa-miR-378g), MIMAT0003326 (hsa-miR-663a), MIMAT0000258 (hsa-miR-181c-5p), MIMAT0000318 (hsa-miR-200b-3p), MIMAT0000095 (hsa-miR-96-5p), MIMAT0014999 (hsa-miR-378b), MIMAT0005870 (hsa-miR-1206), MIMAT0000266 (hsa-miR-205-5p), MIMAT0000460 (hsa-miR-194-5p) and MIMAT0000440 (hsa-miR-191-5p). [score:1]
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