GOLM1 affects proliferation, invasion, and migration by regulating Wnt pathway in esophageal squamous cell carcinoma cells

Aim: To investigate the effect of Golgi membrane protein 1 (GOLM1) on the proliferation, migration, and in-vasion of esophageal squamous cell carcinoma (ESCC) cells and its underlying oncogenic mechanism. Methods: The Expression level of GOLM1 in esophageal cancer (EC) tissues were analyzed in the cancer genome database. Fresh ESCC tissues and cancer adjacent tissues of 44 patients with EC who underwent radical esophagectomy were collected. GOLM1 mRNA expression was detected by RT qPCR. ESCC cell lines (EC9706, TE-1, Eca-109, kyse-150) and normal esophageal epithelial cells (HEEC) were cultured in vitro. Results: The expression level of GOLM1 in EC tissues was significantly higher (P < 0.05). The mRNA expression level of GOLM1 in ESCC was significantly higher than that in adjacent tissues (P < 0.05). Compared with HEEC cells, the mRNA and protein expression levels of GOLM1 in ESCC cell lines were significantly higher (P < 0.05). Kyse-150 cells showed the highest expression of GOLM1. Kyse-150 cells were divided into control group, lenti-NC group, GOLM1 overexpression group, SH-NC group, GOLM1 silencing group, XAV-939 group, and GOLM1 overexpression + XAV-939 group. After lentivirus transfection, the expression levels of mRNA and protein of GOLM1 were significantly higher (P<0.05). In the GOLM1 silence group, all these variables were significantly decreased. Overexpression of GOLM1 can increase the expression of Wnt3a and nuclear beta-catenin and can reverse the effect of XAV-939 intervention. The effect of GOLM1 silence was consistent with that of the XAV-939 intervention. Compared with the NC group, the tumor volume and tumor index of the GOLM1 knockdown group decreased significantly in vivo (P < 0.05). Conclusion: GOLM1 is up-regulated in ESCC tissues and ESCC cells and may function as an oncogene. GOLM1 silencing can reduce the proliferation, migration, and invasion of ESCC cells by inhibiting Wnt/beta-catenin signaling pathway.