中文摘要：

这研究的目的是在房间增长和肺腺癌的 autophagy 调查 apelin 的角色。在肺腺癌的 APJ 的在表示上被 immunohistochemistry 检测，当在肺癌症病人的血浆 apelin 水平被连接酶的 immunosorbent 试金测量时。我们的调查结果表明 apelin-13 显著地增加了 ERK1/2 的 phosphorylation， cyclin D1 的表示，联系微导管的蛋白质 1 轻链 3A/B (LC3A/B ) ，和 beclin1，并且证实 apelin-13 支持了 A549 房间增长并且经由 ERK1/2 发信号导致了 A549 房间 autophagy。而且，人的肺腺癌房间线 A549 的表面和光滑、光滑的 apelin-13 原因房间表面上有毛孔是在原子力量下面观察了显微镜学。这些结果建议 ERK1/2 发信号小径调停 apelin-13-induced 肺腺癌房间增长和 autophagy。在我们的试验性的条件下面，与 3-methyladenine 联系的 autophagy 不涉及房间增长。

英文摘要：

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.