Upregulation of long non coding RNA PCAT-1 contributes to cell proliferation, migration and apoptosis in hepatocellular carcinoma

Wen,Jifeng; Xu,Jun; Sun,Qifeng; Xing,Chengliang; Yin,Wenzhe

doi:10.3892/mmr.2016.5075

Upregulation of long non coding RNA PCAT-1 contributes to cell proliferation, migration and apoptosis in hepatocellular carcinoma

Authors:
- Jifeng Wen
- Jun Xu
- Qifeng Sun
- Chengliang Xing
- Wenzhe Yin
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Affiliations: Department of Gastroenterology, The Second Affiliated Hospital, Harbin Medical University, Harbin, Heilongjiang 150086, P.R. China, Department of Orthopedic Surgery, The Second Affiliated Hospital, Harbin Medical University, Harbin, Heilongjiang 150086, P.R. China
Published online on: March 30, 2016 https://doi.org/10.3892/mmr.2016.5075
Pages: 4481-4486

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Abstract

Long non-coding RNAs (lncRNAs) exert regulatory functions on various biological processes in cancer cells, including proliferation, apoptosis and mobility. Prostate cancer-associated transcript 1 (PCAT-1) is a novel lncRNA that promotes cell proliferation in prostate cancer, however, the effect of PCAT‑1 in hepatocellular carcinoma (HCC) remains to be elucidated. The present study hypothesized that PCAT‑1 also exerts an important effect in HCC. The current study investigated PCAT-1 expression levels in HCC tissue samples and HepG2 and Bel‑7402 cell lines using the reverse transcription-quantitative polymerase chain reaction. The results demonstrated that PCAT-1 was upregulated in HCC tissue samples and cell lines compared with adjacent non‑cancerous tissues and the L02 normal liver epithelial cell line. PCAT‑1 suppression using PCAT‑1 small hairpin RNA in HepG2 and Bel‑7402 cells inhibited cell proliferation and migration, and induced apoptosis. Overexpression of PCAT‑1 induced synthetic plasmid vectors was demonstrated to increase cell proliferation and migration, and inhibit apoptosis. Results from the present study suggest that PCAT‑1 exerts an oncogenic effect in HCC and silencing PCAT-1 may be a potential novel therapeutic strategy for HCC.

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