Berberine Inhibits Proliferation and Induces Apoptosis of Esophageal Cancer Cells via Inactivation of IGF-1R Signaling Pathway

• Main Authors: LI Saisai, GUO Xiaofang, ZHU Xiaofei, DOU Qiaohua
• Format: Article
• Language: zho
• Published: Magazine House of Cancer Research on Prevention and Treatment 2018-06-01
• Series: Zhongliu Fangzhi Yanjiu
• Subjects: berberine; esophageal cancer cells; insulin-like growth factor 1 receptor; cell apoptosis
• Online Access: http://html.rhhz.net/ZLFZYJ/html/8578.2018.17.1500.htm
• ISSN: 1000-8578; 1000-8578

Objective To investigate the effects of berberine on the proliferation, cell cycle progression and apoptosis of esophageal cancer cells and related mechanism. Methods MTT assay was used to evaluate the effects of berberine on cell viability. Propidium iodide staining was used to detect cell cycle progression. Annexin V-FITC/PI staining assay was used to measure cell apoptosis, and Western blot analysis was performed to determine the phosphorylation of insulin-like growth factor 1 receptor (IGF-1R) as well as the two major downstream signaling molecules AKT and p42/44MAPK(ERK). Results In vitro, berberine inhibited the proliferation of four esophageal cancer cell lines in a concentration-dependent manner. Moreover, the IC50 values of berberine against different esophageal cancer cells were negatively correlated with the expression level of IGF-1R. The distribution of KYSE450 cells cycle was arrested in G2/M phase. Berberine dose-dependently induced the cell apoptosis, and the apoptosis ratio of KYSE450 cells with high IGF-1R level was significantly higher than that of KYSE150 cells with low IGF-1R level after berberine treatment at the same concentration. Berberine dose-dependently inhibited the phosphorylation of IGF-1R and blocked AKT and ERK activation. Conclusion Berberine could inhibit cell proliferation, cell cycle arrest and induce cell apoptosis of esophageal cancer via inactivation of IGF-1R as well as the downstream molecules AKT and ERK.