Carcinogenesis, Teratogenesis & Mutagenesis ›› 2018, Vol. 30 ›› Issue (6): 430-434.doi: 10.3969/j.issn.1004-616x.2018.06.003

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Induction of apoptosis in HepG2 hepatocellular carcinoma cells by chloroquine via the P38MAPK pathway

DING Wenping1, LU Yuanyuan1, TONG Wenxia1, ZHOU Aibin1, KONG Xiang2, CHEN Yihong1   

  1. 1. Department of Radiotherapy, Yijishan Hospital Affiliated to Wannan Medical College, Wuhu 241001;
    2. Department of Endocrinology, Yijishan Hospital Affiliated to Wannan Medical College, Wuhu 241001, Anhui, China
  • Received:2018-08-14 Revised:2018-10-15 Online:2018-11-30 Published:2018-11-30

Abstract: OBJECTIVE: To investigate effects of chloroquine on cell proliferation and apoptosis of a hepatocellular carcinoma cell line,HepG2. METHODS: Cultured HepG2 cells were treated with various concentrations of chloroquine (0,10,20 and 40 μmol/L). Cell viability was determined by the MTT assay. Morphological changes in cell nuclei was detected using fluorescence microscope at 24 h after treatment. Cell apoptosis was detected by flow cytometry. Expression levels of Caspase-3,Bcl-2,Bax,P-P53,P38MAPK and P-P38MAPK were performed using Western blot analyses. RESULTS: After treatment with 10-40 μmol/L chloroquine for 24,48 and 72 h,proliferation of HepG2 cells was significantly inhibited compared with the control group (P < 0.05). In addition,treatment with 10,20 and 40 μmol/L led to a significant increase in nuclear concentration and shrinkage. Flow cytometry analyses showed that 10,20 and 40 μmol/L treatment significantly induced apoptosis (P < 0.05). Increased in protein expression of P-P53,P-P38MAPK,cleaved Caspase-3 and Bax was detected in the 20 and 40 μmol/L groups while Caspase-3 and P38MAPK did not change. Expression of Bcl-2 was decreased after treatment with 20 and 40 μmol/L. CONCLUSION: Chloroquine inhibited HepG2 cell growth and induced apoptosis. The underlying mechanism might involve the P38MAPK signaling pathway.

Key words: chloroquine, hepatocellular carcinoma, apoptosis, P38MAPK pathway, P53

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