GOLPH3 Promotes Angiogenesis of Lung Adenocarcinoma by Regulating the Wnt/β-Catenin Signaling Pathway

GOLPH3 promotes proliferation capacity in LADC through activating the Wnt/β-catenin signaling pathway.

The level of GOLPH3 was performed by quantitative real time (qRT)-PCR, Western blot and immunohistochemistry. Patient survival rate was analyzed by Kaplan-Meier method. MTT was used to detect cell viability. The levels of p-serine/threonine-protein kinase (Akt), Akt, p-p65, p65 and β-catenin were determined by Western blot. Cell apoptosis was tested using flow cytometry. Angiogenesis was determined by in vitro angiogenesis assay. qPCR and Western blot were performed to identify apoptotic protein B-cell lymphoma 2 (Bcl-2)/Bcl-2-associated X protein (Bax) and vascular endothelial growth factor (VEGF).

We aim to investigate the role of Golgi phosphoprotein 3 (GOLPH3) and the possible regulation mechanism underlying lung adenocarcinoma (LADC).

GOLPH3 was highly expressed in LADC cell lines and tissues and was significantly correlated with poor overall survival among patients with LADC. Furthermore, GOLPH3 expression was reduced in A549 and H23 cells in a cisplatin-dependent manner. Silencing of GOLPH3 enhanced inhibition of A549 and H23 cells by cisplatin and suppressed the protein expression of p-Akt, while p-p65 expression remained stable. However, overexpression of GOLPH3 weakened the inhibition of A549 and H23 cells by cisplatin and improved the protein expression of p-Akt, while p-p65 expression remained stable. XAV939, an inhibitor of Wnt/β-catenin signaling pathway, decreased GOLPH3 overexpression-induced proliferation and enhanced cisplatin-induced angiogenesis inhibition and apoptosis, which was supported by the changes of VEGF, Bax and Bcl-2.