Mir-184 Post-Transcriptionally Regulates SOX7 Expression and Promotes Cell Proliferation in Human Hepatocellular Carcinoma

Wu, Geng-Gang; Li, Wenhong; He, Wenguang; Jiang, Nan; Zhang, Guang‐Xian; Chen, Wei; Yang, Haifeng; Liu, Qilong; Huang, Yanhui; Zhang, Lei; Zhang, Tong; Zhang, Xiancheng

doi:10.1371/journal.pone.0088796

Cited by 61 publications

(55 citation statements)

References 36 publications

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“…In addition, miR-506 regulates expression of PPAR alpha in hydroxycamptothecin-resistant human colon cancer cells [35] . MiR-184 posttranscriptionally regulates SOX7 expression and promotes proliferation in human hepatocellular carcinoma cells [36] . Our group has reported that miR-205 modulates abnormal lipid metabolism of hepatoma cells via targeting acyl-CoA synthetase long-chain family member 1 and 4 (ACSL1 and ACSL4) mRNA [37,38] .…”

Section: Discussionmentioning

confidence: 99%

MiR-506 suppresses proliferation of hepatoma cells through targeting YAP mRNA 3′UTR

et al. 2014

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Aim: MiR-506 is a miRNA involved in carcinogenesis of several kinds of cancer. In this study, we explored whether miR-506 played a critical role in hepatocellular carcinoma (HCC). Methods: Twenty HCC and adjacent normal liver tissue samples were collected. Human hepatoma cell lines HepG2 and H7402 were used for in vitro studies. The expression of miR-506 and transcriptional co-activator YAP was examined using qRT-PCR. Western blot analysis was used to measure the expression of YAP and its target genes. Luciferase reporter gene assay was used to identify YAP as a target gene of miR-506. MTT and EdU assays were carried out for functional analysis. Results: The expression of miR-506 was significantly lower in HCC than in adjacent normal liver tissues. Bioinformatics analysis revealed that YAP mRNA might be one of the targets of miR-506, and miR-506 in HCC tissues was found to be negatively correlated with YAP (r=-0.605). In both HepG2 and H7402 cells, miR-506 dose-dependently down-regulated YAP and its target genes c-Myc and the connective tissue growth factor (CTGF). Luciferase reporter gene assays demonstrated that miR-506 targeted the wild type 3′UTR of YAP mRNA, but not a 3′UTR with a mutant seed site. Furthermore, miR-506 significantly inhibited the proliferation of HepG2 and H7402 cells, while anti-miR-506 enhanced the cell proliferation, which was blocked by YAP siRNA. Conclusion: MiR-506 suppresses the proliferation of hepatoma cells by targeting YAP mRNA.

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Section: Discussionmentioning

confidence: 99%

MiR-506 suppresses proliferation of hepatoma cells through targeting YAP mRNA 3′UTR

et al. 2014

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“…Decreased miR-184 expression levels were noted in gliomal cells [14,15], central nervous system lymphoma cells [16] and renal cell carcinoma [17]. By contrast, miR-184 expression was found to be upregulated in pancreatic ductal adenocarcinoma [18], hepatocellular carcinoma [19] and tongue squamous cell carcinoma [20]. In a previous study, dysregulated miR-184 contributed to growth and apoptosis [21].…”

Section: Introductionmentioning

confidence: 99%

miR-184 Inhibits Tumor Invasion, Migration and Metastasis in Nasopharyngeal Carcinoma by Targeting Notch2

Zhu¹,

Jiang

et al. 2018

Cell Physiol Biochem

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Background/Aims: A recent study found that dysregulated microRNA-184 (miR-184) is involved in the proliferation and survival of nasopharyngeal carcinoma (NPC). This study aimed to evaluate the detailed mechanisms of invasion, migration and metastasis of NPC cells. Methods: Quantitative reverse-transcription PCR (qRT-PCR) and Western blot were used to confirm the expression levels of miR-184 and Notch2. NPC cell invasion and migration were subsequently examined using in vitro cell invasion and wound-healing assays, respectively. MicroRNA (miRNA) target gene prediction databases and dual-luciferase reporter assay were adopted to validate the target genes of miR-184. Results: MiR-184 was downregulated in the NPC cell lines. The miR-184 inhibitor increased the number of invading NPC cells, whereas miR-184 mimics inhibited the invasive ability of such cells. The protein level of E-cadherin decreased, whereas those of N-cadherin and vimentin increased in the anti-miR-184 group. This result showed that miR-184 inhibited NPC cell invasion and metastasis by regulating EMT progression. MiRNA target gene prediction databases indicated the potential of Notch2 as a direct target gene of miR-184. Such a notion was then validated by results of dual-luciferase reporter assay. Notably, shRNANotch2 restrained the EMT and partially abrogated the inhibitory effects of miR-184 on EMT progression in NPC cells. Conclusion: MiR-184 functions as a tumour-suppressive miRNA targeting Notch2 and inhibits the invasion, migration and metastasis of NPC.

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“…A number of studies have revealed the miRNA profiling of HCC [7,8]. Many miRNAs have been aberrantly altered in HCC and function as oncogenes or tumor suppressors [9,10]. MiR-141 acts as tumor suppressor in several cancers and was deregulated in HCC as well [11,12]; however, its detailed role in HCC remains unclear.…”

Section: Introductionmentioning

confidence: 99%

miR-141 suppresses the growth and metastasis of HCC cells by targeting E2F3

et al. 2014

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MicroRNAs (miRNAs) function as essential post-transcriptional modulators of gene expression involved in a wide range of physiologic and pathologic states, including cancer. Numerous miRNAs have been deregulated in hepatocellular carcinoma (HCC). Here, we investigated the role of miR-141 in HCC. Decreased expression of miR-141 was observed in both HCC tissues and cell lines. Ectopic overexpression of miR-141 reduced proliferation, migration, and invasion of HCC cells. E2F transcription factor 3 (E2F3) was confirmed to be a target of miR-141 in HCC cells. Moreover, restoration of E2F3 significantly reversed the tumor suppressive effects of miR-141. Our results suggest a critical role of miR-141 in suppressing metastasis of HCC cells by targeting E2F3.

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Mir-184 Post-Transcriptionally Regulates SOX7 Expression and Promotes Cell Proliferation in Human Hepatocellular Carcinoma

Cited by 61 publications

References 36 publications

MiR-506 suppresses proliferation of hepatoma cells through targeting YAP mRNA 3′UTR

MiR-506 suppresses proliferation of hepatoma cells through targeting YAP mRNA 3′UTR

miR-184 Inhibits Tumor Invasion, Migration and Metastasis in Nasopharyngeal Carcinoma by Targeting Notch2

miR-141 suppresses the growth and metastasis of HCC cells by targeting E2F3

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