CXCL17蛋白促进顺铂诱导HepG2肝癌细胞自噬形成

目的　探讨CXCL17调节肝癌细胞化疗耐药产生的机制。 方法　构建过表达CXCL17的HepG2细胞系。实验分为过表达CXCL17组，空白质粒组以及对照组。转染的细胞提取总蛋白，Western blot检测蛋白表达状态，流式细胞仪及电镜检测药物作用后的细胞变化。 结果　CXCL17过表达的HepG2细胞株较其亲代细胞对顺铂引起的细胞毒作用和凋亡敏感性下降，但是尚未完全被抑制，而细胞内的自噬增加，线粒体损伤减少，溶酶体增多。 结论　CXCL17通过促进细胞自噬参与调节HepG2细胞的化疗耐药。

Autophagy induces drug resistance in human hepatocellular carcinoma cells line HepG2 by increasing CXCL17 protein expression

Objective　To investigate the mechanism of the development of cisplatin resistance in a hepatocellular carcinoma cell line.　Methods　Over-expression of CXCL17 gene was induced in human hepatocellular carcinoma cells. Western blotting was used to investigate the protein expression of full length CXCL17. Flow cytometry and electron microscopy were used to examine the apoptotic morphological changes after cisplatin treatment in HepG2.　Results　CXCL17 over-expression cells was more resistant to cisplatin-induced cytotoxicity and apoptosis than HepG2 cells. Compared with HepG2 cells, CXCL17 over-expression cells exhibited less apoptosis and more autophagy with decreased CTR1 protein expression. Conclusion　Cisplatin induces drug resistant phenotype by decreasing the protein level of CXCL17, suggesting an autophagic response to cisplatin as a survival mechanism that can promote chemo-resistance.