Wenchao Ma,
Di Zhu,
Tong Yu,
Junwen Xue,
Xiang Sun,
Guofang Zhang,
Yumeng Hou,
Jinrui Li,
Yingzhun Chen,
Hongli Shan,
Haihai Liang
2022, 2(1): 53-64.
doi: 10.2478/fzm-2022-0007
Background Apelin, an endogenous ligand of G-protein coupled receptor (GPCR), is a secreted peptide involved in the development of various tumors. However, the relationship between apelin and nonsmall cell lung cancer (NSCLC) is not quite clear. This study was designed to investigate the effect and mechanism of apelin on cell proliferation, migration and invasion of NSCLC cells. Methods Twelve NSCLC specimens were collected for hematoxylin-eosin (HE) staining and immunohistochemistry analyses. Cell proliferation was examined by 3-(4, 5-Dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide (MTT) and cell migration and invasion were assessed using wound-healing and transwell assays. The subcellular location of yes associated protein 1 (YAP1) in A549 cells was determined by immunofluorescence. The mRNA and protein levels in NSCLC tissues and cell lines were measured by qRT-PCR and western blot, respectively. Results Apelin was upregulated in tumor tissues compared with the adjacent tissues. Apelin promoted proliferation, migration, and invasion of A549 and H460 cells, which was reversed by competitive apelin receptor (APJ) antagonist ML221. Additionally, apelin upregulated YAP1 expression, whereas silence of YAP1 by small interfering RNA (siRNA) attenuated apelin-induced cell proliferation, migration and invasion and suppressed epithelial-mesenchymal transition progression. Conclusion Apelin promotes NSCLC cells proliferation, migration, and invasion by modulating YAP1 and might be a potential therapeutic target for NSCLC treatment.
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