舌鳞癌细胞CAL27自噬诱发索拉菲尼耐药  

Autophagy Induced Chemoresistance of Tongue Squamous Carcinoma Cell CAL27 to Srofeinib

作　　者：刘婷婷 张燎[2] 杨雪峰 张卓 苏荣建 郑华川 黄克强 

机构地区：[1]锦州医科大学附属第二医院口腔科,辽宁锦州121001 [2]泰安市口腔医院口腔科

出　　处：《中国医科大学学报》2016年第9期773-776,782,共5页Journal of China Medical University

基　　金：国家自然科学基金(81172371;81472544);辽宁省科学技术计划(2015408001);辽宁省高等学校优秀人才计划(LJQ2014093);辽宁省自然科学基金(2015020326);辽宁省教育厅科学研究一般项目(L2015325;L2013328)

摘　　要：目的研究舌鳞癌细胞自噬能力对索拉菲尼耐药性的影响。方法将pEGFP-N1-LC3质粒转染入舌鳞癌细胞CAL27,利用MTT观察细胞增殖和耐药,利用Hochest33258染色观察2组细胞核凋亡情况,Western blot检测p-Erk、Atg5、p-Akt蛋白的表达。结果 LC3过表达不影响舌鳞癌细胞增殖(P>0.05),但是LC3高表达的CAL27细胞对索拉菲尼的耐药性和凋亡抵抗能力强于对照组(P<0.05)。转染重组LC3质粒后,细胞p-Erk表达升高(P<0.05),而Atg5和p-Akt无变化(P>0.05)。结论转染LC3重组质粒后,舌鳞癌细胞内自噬水平上调,细胞对索拉菲尼敏感性降低,可能与Ras-Raf-1-MEK-ERK通路相关。Objective To study the effects of autophagy activity on the chemoresistance to srofeinib in tongue squamous cell carcinoma cells. Methods The recombinant plasmid pEGFP-N1-LC3 was transfected into tongue squamous cell carcinoma CAI27 cell. MTr was employed to de- tect the proliferation and chemoresistance. Hochest33258 staining was performed to observe the apeptosis, and Western blot was used to evaluate the expression of p-Erk, Atg5 and p-Akt. Results LC3 overexpression didn＇ t influence the proliferation of CAL27 cells （P 〉 0.05）, while in- creased the chemotherapeutic and apoptotic resistance to srofeinib in comparison to the control （P 〈 0.05 ）. LC3 tmnsfection up-regulated the ex- pression of p-Erk （P 〈 0.05 ）, but did not effect the Atg5 and p-Akt expression （P 〉 0.05 ）. Conclusion The autophagy levels were up-regulated and the drug resistance was increased after tmnsfection of LC3 recombinant plasmid, and the mechanism might be related to Ras-Raf-1-MEK-ERK pathway.

关 键 词：舌癌 索拉菲尼 自噬 

分 类 号：R739[医药卫生—肿瘤]