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

Li Yang, Tao Su, Deguan Lv, Feng Xie, Wei Liu, Jiangang Cao, Irshad Ali Sheikh, Xuping Qin, Lanfang Li and Linxi Chen

Acta Biochim Biophys Sin 2014, 46: 100–111; doi: 10.1093/abbs/gmt140

Learning Key Laboratory for Pharmaco-proteomics, Institute of Pharmacy and Pharmacology, University of South China, Hengyang 421001, China

The aim of this study was to investigate the role of apelin in the cell proliferation and autophagy of lung adenocarcinoma. 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 beclin1, and confirmed that apelin-13 promoted A549 cell proliferation and induced A549 cell autophagy via ERK1/2 signaling. Moreover, there are pores on the surface of human lung adenocarcinoma cell line A549 and apelin-13 causes cell surface smooth and glossy as observed under atomic force microscopy. 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.

图例: Apelin信号通路

全文: http://abbs.oxfordjournals.org/content/46/2/100.full

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