Xun Gou1,1, Xiyan Zhao2,1, Zhengrong Wang1. 1. Key Laboratory of Chronobiology, West China School of Preclinical and Forensic Medicine, Sichuan University, Chengdu, Sichuan 610041, China. 2. Laboratory of Human Function, Hainan Medical University, Haikou, Hainan 571199, China.
Abstract
BACKGROUND: Long noncoding RNAs (lncRNA) have been verified to be involved in hepatocellular carcinoma (HCC) progression. However, the potential biologic function of PVT1 in HCC is not still fully known. METHODS: PVT1 and miR-214 were detected by qRT-PCR assays in HCC tissues and adjacent normal tissues. CCK8, cell colony and transwell invasion assays were performed to evaluate cell proliferation and invasion abilities. Western-blot assay was performed to detect the protein of E-cadherin and Vimentin. QRT-PCR, RNA immunoprecipitation (RIP) and chromatin immunoprecipitation (ChIP) assays demonstrated PVT1 regulated miR-214 expression. RESULTS: The results showed that PVT1 was increased in HCC tissues and higher PVT1 expression was associated with tumor size, histological differentiation grade and advanced TNM stage. Furthermore, we revealed that PVT1 promoted cell proliferation and invasion in HCC. RIP and ChIP assays demonstrated that PVT1 significantly inhibited miR-214 expression by interacting with enhancer of zeste homolog 2 (EZH2). CONCLUSIONS: Thus, these results demonstrated that PVT1/EZH2/miR-214 regulatory pathway might serve as new target for HCC treatment.
BACKGROUND: Long noncoding RNAs (lncRNA) have been verified to be involved in hepatocellular carcinoma (HCC) progression. However, the potential biologic function of PVT1 in HCC is not still fully known. METHODS:PVT1 and miR-214 were detected by qRT-PCR assays in HCC tissues and adjacent normal tissues. CCK8, cell colony and transwell invasion assays were performed to evaluate cell proliferation and invasion abilities. Western-blot assay was performed to detect the protein of E-cadherin and Vimentin. QRT-PCR, RNA immunoprecipitation (RIP) and chromatin immunoprecipitation (ChIP) assays demonstrated PVT1 regulated miR-214 expression. RESULTS: The results showed that PVT1 was increased in HCC tissues and higher PVT1 expression was associated with tumor size, histological differentiation grade and advanced TNM stage. Furthermore, we revealed that PVT1 promoted cell proliferation and invasion in HCC. RIP and ChIP assays demonstrated that PVT1 significantly inhibited miR-214 expression by interacting with enhancer of zeste homolog 2 (EZH2). CONCLUSIONS: Thus, these results demonstrated that PVT1/EZH2/miR-214 regulatory pathway might serve as new target for HCC treatment.
Entities:
Keywords:
Hepatocellular carcinoma; PVT1; enhancer of zeste homolog 2; long non-coding RNA; miR-214