Effect of Apatinib on Invasion and Migration of Lung Cancer Cells
and Its Mechanism.
10.3779/j.issn.1009-3419.2019.05.02
- Author:
Yin YUAN
1
;
Hao GONG
1
;
Yongwen LI
2
;
Hongbing ZHANG
1
;
Ying LI
2
;
Weiting LI
1
;
Pan WANG
1
;
Ruifeng SHI
1
;
Hongyu LIU
2
;
Jun CHEN
1
Author Information
1. Department of Lung Cancer Surgery, Tianjin Medical University General Hospital, Tianjin 300052, China.
2. Tianjin Key Laboratory of lung Cancer Metastasis and Tumor Microenvironment, Tianjin Lung Cancer Institute, Tianjin Medical University General Hospital, Tianjin 300052, China.
- Publication Type:Journal Article
- Keywords:
Apatinib;
Invasion;
Lung neoplasms;
Migration
- MeSH:
Antineoplastic Agents;
pharmacology;
Cell Line, Tumor;
Cell Movement;
drug effects;
Humans;
Lung Neoplasms;
pathology;
Neoplasm Invasiveness;
Pyridines;
pharmacology
- From:
Chinese Journal of Lung Cancer
2019;22(5):264-270
- CountryChina
- Language:Chinese
-
Abstract:
BACKGROUND:Lung cancer is one of the most deadly cancers in the world for human. In recent years, the effect of targeted therapy has become increasingly significant. Apatinib is a multi-target anti-tumor drug that is currently under study. The purpose of this study is to investigate the effects of Apatinib on the biological characteristics of lung cancer cells and its possible mechanism.
METHODS:Lung cancer cell lines H1299 and H3255 were cultured in vitro. The effects of Apatinib on proliferation, migration and invasion of H1299 and H3255 cells were detected by cell proliferation assays wound healing assays and Transwell assays. The protein expression related to cancer angiogenesis and invasion was detected by Western blot.
RESULTS:Apatinib significantly inhibited the proliferation, migration and invasion of H1299 and H3255 in a concentration-dependent manner. Western blot showed that with the increasing of drug concentration, VEGF, VEGFR2, N-cadherin, MMP9, MMP2 and Vimentin were down-regulated, and E-cadherin were up-regulated.
CONCLUSIONS:Apatinib can inhibit the invasion and migration of lung adenocarcinoma cells H1299 and H3255. By regulation of epithelial-mesenchymal transition and the expression of matrix metalloproteinase-related proteins.
