Hsa-miR-331-3p inhibits VHL expression by directly targeting its mRNA 3'-UTR in HCC cell lines

Cao, Yiyi; Zhang, Jinnan; Xiong, Dongmei; Wang, Dan; Wu, Ting; Huang, Aiping; Tang, Hua

doi:10.18388/abp.2014_779

Cited by 13 publications

(8 citation statements)

References 24 publications

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“…MiR-331-3p and miR-338-3p were reported to regulate multiple cancer tumorigenesis and metastasis by targeting many genes in human cells (listed in Supplementary Table 1 , Supplementary Figs. 1 , and 2 ) [ 21 22 23 24 25 26 27 28 29 30 31 32 33 34 35 36 37 38 ]. Therefore, miR-331-3p and miR-338-3p were chosen for further studies.…”

Section: Resultsmentioning

confidence: 99%

LncRNA XLOC_006390 facilitates cervical cancer tumorigenesis and metastasis as a ceRNA against miR-331-3p and miR-338-3p

2018

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ObjectiveCervical cancer is one of the most common malignant tumors. Our previous results showed that long non-coding RNA (lncRNA) XLOC_006390 plays an important role in cervical cancer. In this study, we have explored the mechanism of action of lncRNA XLOC_006390.MethodsLncRNA XLOC_006390 was proposed to exercise its function as a competing endogenous RNA (ceRNA), and its potential targeted miRNAs was predicted through the database LncBase Predicted v.2. Two miRNAs, miR-331-3p, and miR-338-3p, were chosen for the study. Expression of miRNAs and lncRNA in cervical cancer cells and tissues was detected by reverse transcription polymerase chain reaction. To determine the correlation, silencing of XLOC_006390, over-expression of miR-331-3p, and miR-338-3p was performed in SiHa and Caski cell lines, respectively.ResultsBased on the interactive effect between miRNA and lncRNA, miR-331-3p and miR-338-3p were significantly downregulated in cervical cancer cells and tissues, and their expression levels were negatively related to that of lncRNA. Our results also showed that the expression of miR-331-3p target gene NRP2, miR-338-3p target genes PKM2, EYA2 was significantly downregulated when the XLOC_006390 was knocked down. Further, XLOC_006390 was found to facilitate cervical cancer tumorigenesis and metastasis by downregulating miR-331-3p and miR-338-3p expression.ConclusionTaken together, our study demonstrated that XLOC_006390 may serve as a ceRNA and reversely regulates the expression of miR-331-3p and miR-338-3p, thus facilitating cervical cancer tumorigenesis and metastasis.

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Section: Resultsmentioning

confidence: 99%

LncRNA XLOC_006390 facilitates cervical cancer tumorigenesis and metastasis as a ceRNA against miR-331-3p and miR-338-3p

2018

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“…As an independent prognostic factor, miR-331-3p was reported to modulate tumor progression. Epis et al (23) found that miR-331-3p inhibited prostate cancer progression with Aurora Kinase inhibitor II cotreatment; Chen et al (24) reported that in hepatocellular carcinoma patients, serum miR-331-3p and miR-182 functioned as therapic biomarkers; Cao et al (25) verified that miR-331-3p suppressed VHL expression in HCC. Given that miRNAs are widely known as tumor regulators, we provide further evidence in this study that miR-331-3p plays important roles in human CRC.…”

Section: Discussionmentioning

confidence: 99%

miR‑331‑3p suppresses cell invasion and migration in colorectal carcinoma by directly targeting NRP2

Zhang

Wang

2019

Oncol Lett

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Colorectal carcinoma (CRC) is a common tumor of the digestive system with poor prognosis. Studies have shown that aberrant microRNA (miRNA) expression can affect CRC progression by regulating target genes. In the present study, we investigated the functional roles and potential mechanisms of miR-331-3p in CRC. The expression of miR-331-3p and neuropilin-2 (NRP2) in CRC was detected by RT-qPCR. Then, Transwell assays were conducted to investigate the influence of miR-331-3p on CRC cell invasion and migration abilities. Luciferase reporter assays were performed to determine the target gene of miR-331-3p. It was found that miR-331-3p expression was notably declined in CRC and inversely correlated with the NRP2 expression. miR-331-3p upregulation significantly inhibited CRC cell invasion and migration. Additionally, western blot analysis demonstrated that miR-331-3p restoration evidently suppressed CRC cell EMT. Moreover, NRP2 was conformed to be a novel target of miR-331-3p and knockdown of NRP2 partially inversed the effects of the miR-331-3p inhibitor on cell invasion and migration. These results suggested that miR-331-3p exerted tumor suppressive roles in CRC by targeting NRP2 and miR-331-3p/NRP2 may serve as a potential therapy for CRC.

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“…It was also demonstrated that miR-566 regulates vascular endothelial growth factor (VEGF) by targeting VHL in human glioblastoma in vitro and in vivo (24). Another study suggested that hsa-miR-331-3p downregulates VHL expression in hepatocellular carcinoma cell lines by targeting its 3'-UTR (25), and that miR-101 targets VHL to promote HIF-1α-mediated apoptosis and cell cycle arrest (26). Similarly, the inhibitory effects of miR-185 on cell proliferation and its activation of cell apoptosis by targeting VEGFA have been attributed to VHL inactivation in clear cell renal cell carcinoma (27).…”

Section: Discussionmentioning

confidence: 99%

MicroRNA‑21‑5p induces the metastatic phenotype of human cervical carcinoma cells in vitro by targeting the von Hippel‑Lindau tumor suppressor

Cai

Wang

et al. 2018

Oncol Lett

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Abstract. Numerous studies have indicated that microRNAs (miRs), a group of small non-coding RNAs, are determining regulatory elements involved in the pathogenesis of various types of cancer, including cervical cancer (CC). Although miR-21-5p upregulation has been demonstrated to associate with tumorigenesis by controlling the expression of oncogenic and tumor suppressor genes, only a small number of studies have investigated the expression of miR-21-5p and its functional role in CC. The objective of the present study was to investigate the effect of miR-21-5p on the proliferation, apoptosis, migration and invasion of CC cells, and the potential underlying molecular mechanism of these effects. The measurement of miR-21-5p levels using quantitative polymerase chain reaction revealed that miR-21-5p was markedly increased in CC cell lines compared with normal cells. Upon silencing of miR-21-5p, a marked suppression of the proliferation, migration and invasion of CaSki cells was observed, with induction of cell apoptosis. These effects were reversed with miR-21-5p overexpression. A database search followed by a luciferase reporter assay ascertained that the 3'-untranslated region of the von Hippel-Lindau tumor suppressor (VHL) mRNA sequence was a direct target of miR-21-5p. Furthermore, silencing of VHL neutralized the effects of miR-21-5p inhibition. These observations suggested that miR-21-5p is an oncogene that is able to promote the metastatic phenotype of CC cells through downregulation of VHL expression, which may present a path to novel therapeutic stratagems for the CC therapy.

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Hsa-miR-331-3p inhibits VHL expression by directly targeting its mRNA 3'-UTR in HCC cell lines

Cited by 13 publications

References 24 publications

LncRNA XLOC_006390 facilitates cervical cancer tumorigenesis and metastasis as a ceRNA against miR-331-3p and miR-338-3p

LncRNA XLOC_006390 facilitates cervical cancer tumorigenesis and metastasis as a ceRNA against miR-331-3p and miR-338-3p

miR‑331‑3p suppresses cell invasion and migration in colorectal carcinoma by directly targeting NRP2

MicroRNA‑21‑5p induces the metastatic phenotype of human cervical carcinoma cells in vitro by targeting the von Hippel‑Lindau tumor suppressor

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