Shao Xin, Liu Yong, Huang Hai, Zhuang Linyuan, Luo Tianping, Huang Huping, Ge Xinguo
Department of Pathology, Changzhou Hospital of Traditional Chinese Medicine, Changzhou, 213003, Jiangsu Province, China.
Cell Biol Int. 2015 Apr;39(4):418-26. doi: 10.1002/cbin.10412. Epub 2015 Jan 13.
G protein-coupled receptors (GPCRs) are important signal transduction mediators and pharmacological therapeutic targets. G protein-coupled receptor 137 (GPR137) was initially reported as a novel orphan GPCR around 10 years ago. Some orphan GPCRs have been implicated in cancer cell proliferation and migration. The aim of this study is to investigate the role of GPR137 in hepatocellular carcinoma (HCC). GPR137 is widely expressed in several human HCC cell lines, as determined by real-time PCR. We then applied lentivirus mediated RNA interference (RNAi) to knock down GPR137 expression in two HCC cell lines HepG2 and Bel7404. Depletion of GPR137 remarkably inhibited cell proliferation and colony formation capacity. Knockdown of GPR137 in HepG2 cells led to cell cycle arrest at G0/G1 phase and G2/M phase, and induced cell apoptosis, as determined by flow cytometry analysis, which contributed to cell growth inhibition. Our findings suggested that GPR137 could facilitate HCC cell proliferation and thus promote hepatocarcinogenesis.
G蛋白偶联受体（GPCRs）是重要的信号转导介质和药理学治疗靶点。大约10年前，G蛋白偶联受体137（GPR137）最初被报道为一种新型孤儿GPCR。一些孤儿GPCR与癌细胞的增殖和迁移有关。本研究的目的是探讨GPR137在肝细胞癌（HCC）中的作用。通过实时PCR测定，GPR137在几种人肝癌细胞系中广泛表达。然后，我们应用慢病毒介导的RNA干扰（RNAi）来敲低两种肝癌细胞系HepG2和Bel7404中GPR137的表达。GPR137的缺失显著抑制了细胞增殖和集落形成能力。通过流式细胞术分析确定，敲低HepG2细胞中的GPR137导致细胞周期停滞在G0/G1期和G2/M期，并诱导细胞凋亡，这有助于抑制细胞生长。我们的研究结果表明，GPR137可以促进肝癌细胞增殖，从而促进肝癌发生。
