Fig. 6: GOLPH3 overexpression enhances EMT of colon cancer cells by inducing autophagy, both in vitro and in vivo.

A GOLPH3-overexpressing and control HCT-116 and HT-29 cells were cultured in regular cell culture solution with or without 50 μM CQ. Western blotting analysis of autophagy inhibition markers (p62 and LC3 II), epithelial markers (E-cadherin), and mesenchymal markers (N-cadherin) was performed. The overexpression of GOLPH3 induced downregulation of p62, LC3 II, and E-cadherin, while it induced upregulation of N-cadherin. When autophagy was suppressed by CQ, E-cadherin levels increased, and N-cadherin levels decreased in each group. B GOLPH3-overexpressing HCT-116 cells and their controls and GOLPH3-silenced HCT-116 cells and their controls were injected into zebrafish and then cultured in medium solution with or without an autophagy suppressor (25 μM CQ). C A decreased quantity of disseminated tumor foci was observed in the GOLPH3-overexpression model (P = 0.0001) and its control (P = 0.0017).