Abstract
背景与目的表皮生长因子受体酪氨酸激酶抑制剂(epidermal growth factor receptor tyrosine kinase inhibitor, EGFR-TKI)的原发和继发性耐药已成为其在临床肺癌治疗中的拦路虎，在肺癌组织中研究发现TRIM24呈高表达状态，在肺癌细胞中能调控细胞增殖、周期和细胞凋亡，本研究旨在进一步探讨TRIM24调控肺癌细胞吉非替尼耐药的分子机制。方法应用MTT方法和流式细胞仪检测干扰TRIM24及干扰TRIM24后加入吉非替尼对肺癌细胞系增殖能力及凋亡率的抑制率的变化，同时应用Western blot方法检测凋亡相关基因的变化及AKT信号通路中蛋白的表达。结果在A549细胞中使用干扰TRIM24可以提高吉非替尼对肿瘤增殖能力的抑制率，增加吉非替尼诱导的凋亡水平，同时干扰TRIM24及干扰TRIM24加入吉非替尼后促凋亡相关基因p-BAD、Bcl-2和AKT及AKT信号通路相关蛋白PIK3CA均出现降低。结论TRIM24能够调控肺癌细胞吉非替尼耐药，并且通过AKT信号通路引起肺癌细胞EGFRTKI耐药。
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