Kin17在非小细胞肺癌侵袭转移中的作用及其机制研究  

The Role and Mechanism of Kin17 in Invasion and Metastasis of Non-small Cell Lung Cancer

作　　者：吕俊宏[1] 彭盘俐[2] 韦文姜[3] 林少欢[1] 曾涛 LV Jun-hong;PENG Pan-li;WEI Wen-jiang;LIN Shao-huan;ZENG Tao(Department of Cardio-Thoracic Surgery,The Second People's Hospital of Guangdong Province,Guangzhou,Guangdong,510037,China;Second Department of Oncology,The Second People's Hospital of Guangdong Province,Guangzhou,Guangdong,510037,China;Department of Interventional,The Second People's Hospital of Guangdong Province,Guangzhou,Guangdong,510037,China;Department of Laboratory,Guangdong Medical University,Zhanjiang,Guangdong,524023,China)

机构地区：[1]广东省第二人民医院心胸外科,广东广州510037 [2]广东省第二人民医院肿瘤二科,广东广州510037 [3]广东省第二人民医院介入科,广东广州510037 [4]广东医科大学检验系,广东湛江524023

出　　处：《现代生物医学进展》2020年第15期2838-2842,共5页Progress in Modern Biomedicine

基　　金：广东省医学科研基金项目(20191119201823122)。

摘　　要：目的:探究核蛋白17(Kin17)在非小细胞肺癌侵袭转移中的作用及其机制研究。方法:采用核糖核苷酸测序(RNA-seq)技术比较A549-KD组细胞与A549-NC组细胞中的信使RNA(mRNA)表达谱,从中筛选出表达差异较大的基因。采用蛋白免疫印迹(Western blot)方法对A549-NC组、A549-KD组和A549-KD+信号转导与转录激活因子3(STAT3)组细胞中Kin17、STAT3、磷酸甘油醛脱氢酶(GAPDH)、E-钙黏蛋白(E-cadherin)、波形蛋白(Vimentin)、碱性螺旋-环-螺旋转录因子(Twist)和转录因子(Snail)表达水平进行检测,采用划痕实验检测细胞侵袭能力,采用Transwell实验检测细胞迁移能力,采用免疫荧光实验检测Kin17和STAT3蛋白在细胞中的定位情况。结果:与A549-NC组相比,A549-KD组的STAT3表达水平下降(P<0.05)。A549-KD组E-cadherin表达水平高于A549-NC组和A549-KD+STAT3组,而Vimentin、Twist和Snail表达水平低于A549-NC组和A549-KD+STAT3组(P<0.05)。A549-KD组划痕愈合率、细胞迁移率低于A549-NC组和A549-KD+STAT3组(P<0.05)。Kin17和STAT3蛋白共定位于细胞核中。结论:在非小细胞肺癌中Kin17可能通过促进STAT3表达水平以促进非小细胞肺癌细胞上皮-间质转化(EMT)、侵袭和转移,Kin17及STAT3在非小细胞肺癌患者诊断和治疗中具有一定临床价值。Objective: To investigate the role and mechanism of Kin17 in invasion and metastasis of non-small cell lung cancer.Methods: The Messenger RNA(m RNA)expression profiles of A549-KD cells and A549-NC cells were compared by Ribonucleotide sequencing(RNA-seq), and the genes with different expressions were screened out.Expression level of Kin17, activator of transcription 3(STAT3), glycerol phosphate aldehyde dehydrogenase(GAPDH), E-cadherin(E-cadherin), Vimentin(Vimentin), Basic helix loop helix transcription factor(Twist)and transcription factor(Snail)in A549-NC group, the A549-KD group and A549-KD+STAT3 group was tested by Western blot( Western blot) Cell invasive ability of each group was detected by scratch experiment. Cell migration ability of each group was detected by Transwell experiment. The position of Kin17 and STAT3 was detected by immunofluorescence experiment.Results: Compared with A549-NC group, STAT3 expression in A549-KD group decreased(P < 0.05). The expression level of E-cadherin in A549-KD group was higher than that in A549-NC group and A549-KD+STAT3 group, while the expression levels of vimentin, twist and snail were lower than that in A549-NC group and a549-kd + STAT3 group(P < 0.05). The scratch healing rate and cell migration rate of a549-kd group were lower than those of a549-nc group and a549-kd + STAT3 group(P < 0.05). Kin17 and STAT3 are Co located in the nucleus. Conclusion: Kin17 may promote EMT, invasion and metastasis of NSCLC cells by promoting the expression level of STAT3 in NSCLC. Kin17 and STAT3 have certain clinical value in the diagnosis and treatment of NSCLC patients.

关 键 词：非小细胞肺癌 侵袭 转移 核蛋白17 信号转导与转录激活因子3 上皮-间质转化 

分 类 号：R-33[医药卫生] R734.2