Learning Key Laboratory for Pharmaco-proteomics, Institute of Pharmacy and Pharmacology, University of South China, Hengyang 421001, China.
Acta Biochim Biophys Sin (Shanghai). 2014 Feb;46(2):100-11. doi: 10.1093/abbs/gmt140. Epub 2013 Dec 29.
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.
本研究旨在探讨 Apelin 在肺腺癌细胞增殖和自噬中的作用。通过免疫组织化学检测肺腺癌中 APJ 的过表达，同时通过酶联免疫吸附试验测量肺癌患者血浆中的 Apelin 水平。我们的研究结果表明，Apelin-13 可显著增加 ERK1/2 的磷酸化、细胞周期蛋白 D1、微管相关蛋白 1 轻链 3A/B（LC3A/B）和 Beclin1 的表达，证实 Apelin-13 通过 ERK1/2 信号通路促进 A549 细胞增殖并诱导 A549 细胞自噬。此外，在原子力显微镜下观察到，人肺腺癌细胞系 A549 的表面有孔，Apelin-13 使细胞表面变得光滑。这些结果表明，ERK1/2 信号通路介导 Apelin-13 诱导的肺腺癌细胞增殖和自噬。在我们的实验条件下，与 3-甲基腺嘌呤相关的自噬不参与细胞增殖。
