The oncogenic role of TRIP13 in regulating proliferation, invasion, and cell cycle checkpoint in NSCLC cells

TRIP13 在调节 NSCLC 细胞增殖、侵袭和细胞周期检查点中的致癌作用

阅读:5
作者:Qiao Zhang, Yan Dong, Shaohuan Hao, Ying Tong, Qin Luo, Patiguli Aerxiding

Abstract

TRIP13 (thyroid hormone receptor interacting protein 13) AAA-ATPase has been reported to be involved in the metaphase checkpoint in human breast cancer, prostate cancer, and cervical cancer. However, the expression pattern and biologic role of TRIP13 in non-small cell lung cancer (NSCLC) remained unknown. In our present study, real-time PCR and western blot were used to detect the expression level of TRIP13 in NSCLC tissues and cell lines. We found that the expression levels of TRIP13 mRNA and protein were significantly upregulated in cell lines and lung tissues. Knockdown of TRIP13 by lentivirus inhibited cell proliferation and invasion in both A549 and H1299 cells. Furthermore, flow cytometry, western blot and immunoprecipitation showed that the MCC complex was disassembled and cells became arrested in metaphase, when TRIP13 was inhibited. In conclusion, here we first report that TRIP13 acts as a tumor promoter in regulating cell proliferation, invasion, and cell cycle checkpoint in NSCLC cells and may be a clinically useful marker for the diagnosis and treatment of lung cancer.

特别声明

1、本页面内容包含部分的内容是基于公开信息的合理引用;引用内容仅为补充信息,不代表本站立场。

2、若认为本页面引用内容涉及侵权,请及时与本站联系,我们将第一时间处理。

3、其他媒体/个人如需使用本页面原创内容,需注明“来源:[生知库]”并获得授权;使用引用内容的,需自行联系原作者获得许可。

4、投稿及合作请联系:info@biocloudy.com。