Abstract

MicroRNA-214 (MiR-214) is aberrantly expressed in several human tumors such as ovarian cancer and breast cancer. However, the role of miR-214 in nasopharyngeal carcinoma (NPC) is still unknown. In this study, we report that miR-214 was overexpressed in NPC cell lines and tissues. Silencing of miR-214 by LNA-antimiR-214 in NPC cells resulted in promoting apoptosis and suppressing cell proliferation in vitro, and suppressed tumor growth in nude mice in vivo. Luciferase reporter assay was performed to identify Bim as a direct target of miR-214. Furthermore, this study showed that low Bim expression in NPC tissues correlated with poor survival of NPC patients. Taken together, our findings suggest that miR-214 plays an important role in NPC carcinogenesis.

Highlights

  • MicroRNAs are small, endogenous and non-coding RNAs, which modulate gene expression by binding to the 39 untranslated region (39 UTR) of target mRNA, and promoting RNA degradation, inhibiting mRNA translation, and affecting transcription [1]

  • MiR-214 is overexpressed in nasopharyngeal carcinoma (NPC) tissues and cell lines We performed fluorescence in situ hybridization (FISH) on 5

  • The overexpression of miR-214 was observed in NPC tissues compared to normal adjacent tissue (NATs)

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Summary

Introduction

MicroRNAs (miRNAs) are small, endogenous and non-coding RNAs, which modulate gene expression by binding to the 39 untranslated region (39 UTR) of target mRNA, and promoting RNA degradation, inhibiting mRNA translation, and affecting transcription [1]. Recent studies have shown that miRNA mutations or abnormal expression in many human cancers, indicating that they may function as tumour suppressor genes (TSG) and oncogenes [3,4,5,6]. They have the potential to regulate various critical biological processes, including the differentiation, apoptosis, proliferation and metastasis of tumor cells [7,8,9]. MiR-214 induces cell survival and cisplatin resistance by binding to 39-UTR of PTEN leading to inhibition of PTEN translation and activation of Akt pathway [21]. MiR-214 promoted survival of pancreatic cancer cells as well as GEM resistance, which might be related to the poor response to chemotherapy in pancreatic cancer patients [17]

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