Met is involved in TIGAR-regulated metastasis of non-small-cell lung cancer

被引：37

作者：

Shen, Mengqin ^{[1
,3
]}

Zhao, Xiaoping ^{[1
,3
]}

Zhao, Li ^{[1
,3
]}

Shi, Liang ^{[1
,3
]}

An, Shuxian ^{[1
,3
]}

Huang, Gang ^{[1
,2
,3
]}

Liu, Jianjun ^{[1
,3
]}

机构：

[1] Shanghai Jiao Tong Univ, Sch Med, Ren Ji Hosp, Dept Nucl Med, Shanghai 200127, Peoples R China

[2] Shanghai Univ Med & Hlth Sci, Collaborat Sci Res Ctr, Shanghai Key Lab Mol Imaging, Shanghai 200093, Peoples R China

[3] Shanghai Jiao Tong Univ, Inst Nucl Med, Sch Med, Shanghai 200127, Peoples R China

来源：

MOLECULAR CANCER | 2018年 / 17卷

基金：

中国国家自然科学基金;

关键词：

TIGAR; Met; Non-small-cell lung cancer; Metastasis; Epithelial-mesenchymal transition; TP53-INDUCED GLYCOLYSIS; APOPTOSIS REGULATOR; C-MET; OXIDATIVE STRESS; METABOLISM; IDENTIFICATION; PROGRESSION; ACTIVATION; PATHWAYS; RECEPTOR;

D O I：

10.1186/s12943-018-0839-4

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

TIGAR is a p53 target gene that is known to protect cells from ROS-induced apoptosis by promoting the pentose phosphate pathway. The role of TIGAR in tumor cell invasion and metastasis remains elusive. Here we found that downregulation of TIGAR reduced the invasion and metastasis of NSCLC cells in vitro and in vivo. Immunohistochemical analysis of 72 NSCLC patients showed that TIGAR and Met protein expression was positively correlated with late stages of lung cancer. Besides, patients with high co-expression of TIGAR and Met presented a significantly worse survival. In addition, we found that Met signaling pathway is involved in TIGAR-induced invasion and metastasis. Our study indicates that TIGAR/Met pathway may be a novel target for NSCLC therapy. It is necessary to evaluate the expression of TIGAR before Met inhibitors are used for NSCLC treatment.

引用

页数：12