长链非编码 RNA PVT1 通过调节 miR-214 促进肝癌进展。
Long noncoding RNA PVT1 promotes hepatocellular carcinoma progression through regulating miR-214.
机构信息
Key Laboratory of Chronobiology, West China School of Preclinical and Forensic Medicine, Sichuan University, Chengdu, Sichuan 610041, China.
Laboratory of Human Function, Hainan Medical University, Haikou, Hainan 571199, China.
出版信息
Cancer Biomark. 2017 Dec 6;20(4):511-519. doi: 10.3233/CBM-170331.
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.
背景
长链非编码 RNA（lncRNA）已被证实参与肝细胞癌（HCC）的进展。然而，PVT1 在 HCC 中的潜在生物学功能仍不完全清楚。
方法
采用 qRT-PCR 法检测 HCC 组织和相邻正常组织中的 PVT1 和 miR-214。CCK8 法、细胞集落形成实验和 Transwell 侵袭实验分别用于评估细胞增殖和侵袭能力。Western-blot 法检测 E-钙黏蛋白和波形蛋白的蛋白表达。QRT-PCR、RNA 免疫沉淀（RIP）和染色质免疫沉淀（ChIP）实验证实 PVT1 调节 miR-214 的表达。
结果
结果表明，PVT1 在 HCC 组织中表达上调，且高 PVT1 表达与肿瘤大小、组织学分化程度和晚期 TNM 分期相关。此外，我们揭示了 PVT1 可促进 HCC 细胞的增殖和侵袭。RIP 和 ChIP 实验表明，PVT1 通过与增强子结合抑制 miR-214 的表达。
结论
因此，这些结果表明，PVT1/EZH2/miR-214 调控通路可能成为 HCC 治疗的新靶点。
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