Research Papers:

Regulation of p53 expression and apoptosis by vault RNA2-1-5p in cervical cancer cells

Lu Kong, Qi Hao, Ying Wang, Ping Zhou, Binbin Zou and Yu-xiang Zhang _

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Oncotarget. 2015; 6:28371-28388. https://doi.org/10.18632/oncotarget.4948

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Lu Kong1, Qi Hao1, Ying Wang1, Ping Zhou2, Binbin Zou1 and Yu-xiang Zhang1,3,4

1 Department of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Capital Medical University, Beijing, China

2 Department of Bioinformatics and Computer Science, School of Biomedical Engineering, Capital Medical University, Beijing, China

3 Cancer Institute of Capital Medical University, Beijing, China

4 Beijing Key Laboratory for Cancer Invasion and Metastasis Research, Capital Medical University, Beijing, China

Correspondence to:

Yu-xiang Zhang, email:

Keywords: non-coding microRNAs, p53, cervical cancer, VTRNA2-1-5p, apoptosis

Received: December 17, 2014 Accepted: July 02, 2015 Published: July 22, 2015


nc886 or VRNA2-1 has recently been identified as a noncoding RNA instead of a vault RNA or a pre-microRNA. Several studies have reported that pre-miR-886 plays a tumor-suppressive role in a wide range of cancer cells through its activity as a cellular protein kinase RNA-activated (PKR) ligand and repressor. However, by sequencing stem-PCR products, we found that a microRNA originating from this precursor, vault RNA2-1-5p (VTRNA2-1-5p), occurs in cervical cancer cells. The expression levels of the predicted targets of VTRNA2-1-5p are negatively correlated with VTRNA2-1-5p levels by quantitative reversion transcription PCR (qRT-PCR). Previous results have shown that VTRNA2-1-5p is overexpressed in human cervical squamous cell carcinomas (CSCCs) compared with adjacent healthy tissues. Inhibition of VTRNA2-1-5p increases Bax protein expression and apoptotic cell death in cervical cancer cells. Our findings suggest that VTRNA2-1-5p has oncogenic activity related to the progression of cervical cancer. Here, we report that VTRNA2-1-5p directly targeted p53 expression and functioned as an oncomir in cervical cancer. VTRNA2-1-5p inhibition decreased cervical cancer cell invasion, proliferation, and tumorigenicity while increasing apoptosis and p53 expression. Interestingly, VTRNA2-1-5p inhibition also increased cisplatin-induced apoptosis of HeLa and SiHa cells. In human clinical cervical cancer specimens, low p53 expression and high VTRNA2-1-5p expression were positively associated.In addition, VTRNA2-1-5p was found to directly target the 5′ and 3′ untranslated regions (UTRs) of p53. We propose that VTRNA2-1-5p is a direct regulator of p53 and suggest that it plays an essential role in the apoptosis and proliferation of cervical cancer cells.

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