ERK1/2 mediates lung adenocarcinoma cell proliferation and autophagy induced by apelin-13  

作　　者：Li Yang Tao Su Deguan Lv FengXie Wei Liu Jiangang Cao Irshad Ali Sheikh Xuping Qin Lanfang Li Linxi Chen 

机构地区：[1]Learning Key Laboratory for Pharmaco-proteomics, Institute of Pharrnacy and Pharmacology, University of South China,Hengyang 421001, China [2]Department of Pharmacy, First People's Hospital of Jingzhou, First Affiliated Hospital of Yangtze University, Jingzhou 434000, China [3]Molecular Pathophysiology Division, National Institute of Cholera and Enteric Diseases, Kolkata 700010, India

出　　处：《Acta Biochimica et Biophysica Sinica》2014年第2期100-111,共12页生物化学与生物物理学报（英文版）

基　　金：This work was supported by the grants from the National Natural Science Foundation of China （81270420, 30901577）, the Scientific Research Foundation for the Retumed Overseas Chinese Scholars, State Education Ministry （20091590）, the Hengyang Joint Funds of Hunan Provincial Natural Science Foundation of China （12JJ8013）, Hunan Provincial Natural Science Foundation of China （14JJ3102）, the Open Fund Project of Key Laboratory in Hunan Universities （10K051）, and the Construct Program of the Key Discipline in Hunan Province.

摘　　要：The aim of this study was to investigate the role of apelin in the cell proliferation and autophagy of lung adenocarcin- oma. The over-expression of APJ in lung adenocarcinoma was detected by immunohistochemistry, while plasma apelin level in lung cancer patients was measured by enzyme-linked immunosorbent assay. Our findings revealed that apelin-13 significantly increased the phosphorylation of ERK1/2, the expression of cyclin D1, microtubule-associated protein 1 light chain 3A/B （LC3A/B）, and beclinl, and con- fwmed that apelin-13 promoted A549 cell proliferation and induced A549 cell autophagy via ERK1/2 signaling. More- over, there are pores on the surface of human lung adeno- carcinoma cell line A549 and apelin-13 causes cell surface smooth and glossy as observed under atomic force micros- copy. These results suggested that ERK1/2 signaling pathway mediates apelin-13-induced lung adenocarcinoma cell proliferation and autophagy. Under our experimental condition, autophagy associated with 3-methyladenine was not involved in cell proliferation.The aim of this study was to investigate the role of apelin in the cell proliferation and autophagy of lung adenocarcin- oma. The over-expression of APJ in lung adenocarcinoma was detected by immunohistochemistry, while plasma apelin level in lung cancer patients was measured by enzyme-linked immunosorbent assay. Our findings revealed that apelin-13 significantly increased the phosphorylation of ERK1/2, the expression of cyclin D1, microtubule-associated protein 1 light chain 3A/B （LC3A/B）, and beclinl, and con- fwmed that apelin-13 promoted A549 cell proliferation and induced A549 cell autophagy via ERK1/2 signaling. More- over, there are pores on the surface of human lung adeno- carcinoma cell line A549 and apelin-13 causes cell surface smooth and glossy as observed under atomic force micros- copy. These results suggested that ERK1/2 signaling pathway mediates apelin-13-induced lung adenocarcinoma cell proliferation and autophagy. Under our experimental condition, autophagy associated with 3-methyladenine was not involved in cell proliferation.

关 键 词：APELIN APJ lung adenocarcinoma ERK1/2 proliferation AUTOPHAGY 

分 类 号：Q253[生物学—细胞生物学] S663.101[农业科学—果树学]