摘要
目的:探讨TM6SF1基因在肺腺癌细胞中的作用。方法:通过GEPIA数据库分析TM6SF1基因在肺腺癌及正常组织中的表达情况;细胞增殖实验检测过表达TM6SF1后,A549细胞的增殖情况;细胞划痕实验检测过表达TM6SF1后,A549细胞伤口愈合情况;Transwell细胞实验检测过表达TM6SF1后,A549细胞侵袭和迁移情况。结果:通过GEPIA数据库分析得知,与正常组织相比,TM6SF1在肺腺癌中的表达降低,差异有统计学意义(^(*)P<0.05,^(**)P<0.01,^(***)P<0.001),且高表达TM6SF1组生存期更长。另外,TM6SF1与细胞增殖相关的核抗原Ki-67具有负相关性。过表达TM6SF1后,A549细胞的增殖,侵袭和迁移都受到抑制,差异有统计学意义(^(*)P<0.05,^(**)P<0.01,^(***)P<0.001),且下调细胞中信号(PI3K/Akt)通路相关激酶的表达。结论:TM6SF1基因在肺腺癌中可能作为抑癌因子。
Objective:To investigate the role of TM6SF1 gene in lung adenocarcinoma cells.Methods:The expression of TM6SF1 gene in lung adenocarcinoma and normal tissues was analyzed by GEPIA database.Cell proliferation assay was performed to detect the proliferation of A549 cells after overexpression of TM6SF1.Wound-healing?assay was used to test the speed of wound healing after over-expressing TM6SF1.Transwell cell assay to detect A549 cell invasion and migration after overexpression of TM6SF1.Results:Analysis of the GEPIA database revealed that the expression of TM6SF1 was reduced in lung adenocarcinoma compared with normal tissues,with statistically significant difference(^(*)P<0.05,^(**)P<0.01,^(***)P<0.001),and the survival was longer in the group with high expression of TM6SF1.TM6SF1 negatively correlated with the cell proliferation-associated nuclear antigen Ki-67.After overexpression of TM6SF1,the proliferation,invasion and migration of A549 cells were inhibited,with statistically significant difference(^(*)P<0.05,^(**)P<0.01,^(***)P<0.001),and the expression of PI3K/Akt pathway-associated kinases was down-regulated.Conclusion:The TM6SF1 gene may act as an oncogenic factor in lung adenocarcinoma.
作者
刘婷隽
Liu Tingjun(Center of Animal Laboratory,Xuzhou Medical University,Xuzhou,Jiangsu,221004,China)
出处
《黑龙江医学》
2023年第23期2837-2840,共4页
Heilongjiang Medical Journal
基金
徐州市科技局2021年社会发展项目(KC21258)。
关键词
肺腺癌细胞
TM6SF1基因
增殖
迁移
侵袭
Lung adenocarcinoma cells
TM6SF1gene
Proliferation
Migration
Invasion
