C6orf106促进肺癌细胞的侵袭和增殖  

C6orf106 promote the proliferation and invasive ability of lung cancer cells

作　　者：姜贵洋[1] 张冲[1] 张秀鹏[1] 徐洪涛[1] 王恩华[1] 

机构地区：[1]中国医科大学基础医学院病理学教研室附属第一医院病理科,辽宁沈阳110001

出　　处：《解剖科学进展》2016年第3期256-258,262,共4页Progress of Anatomical Sciences

基　　金：国家自然科学基金(81402369;81272606)

摘　　要：目的探讨C6orf106(chromosome 6 open reading frame 106)对肺癌细胞中侵袭和增殖能力的影响。方法分别在肺癌细胞A549和SPC细胞中转染和干扰C6orf106的表达,Transwell和MTT检测细胞侵袭和增殖能力的改变,同时Western Blot检测E-cadherin、c-myc、cyclin A2和cyclin B1等一系列侵袭、增殖相关因子的改变。结果转染外源性的C6orf106可促进A549细胞的侵袭和增殖能力,而si RNA干扰C6orf106可抑制SPC细胞的侵袭和增殖能力。C6orf106可以调控E-cadherin、c-myc、cyclin A2和cyclin B1等侵袭、增殖相关因子的表达水平。结论 C6orf106能够促进肺癌细胞的侵袭和增殖,且这种作用可能通过调控E-cadherin、c-myc、cyclin A2和cyclin B1等侵袭、增殖相关因子的表达而实现的。Objective To investigate the effects of C6orf106（chromosome 6 open reading frame 106） on invasion and proliferation ability of the lung cancer cells. Methods After transfection and interference of C6orf106 respectively in A549 and SPC cells, Transwell and MTT were used to detect the invasion and proliferation ability of the lung cancer cells, meanwhile, the expression of some invasion and proliferation related factors, such as, E-cadherin, c-myc, cyclin A2 and cyclin B1, was detected by Western Blot. Results Transfection of C6orf106 promoted the proliferation and invasion of A549, and interference of C6orf106 inhibited the proliferation and invasion of SPC; Furthermore, C6orf106 regulated the expression of E-cadherin, c-myc, cyclin A2 and cyclin B1. Conclusion The overexpression of C6orf106 could promote the proliferation and invasion of lung cancer cells, which might be related to the downregulation of E-cadherin and the upregulation of c-myc, cyclin A2 and cyclin B1.

关 键 词：C6orf106 非小细胞肺癌 

分 类 号：R734.2[医药卫生—肿瘤]