GOLM1 facilitates human colorectal cancer progression and metastasis via activating the AKT/GSK3β/EMT axis.

GOLM1 (Golgi membrane protein 1), a key tumor progression- and metastasis-related marker, is highly expressed in a variety of epithelium-derived human cancers. However, its expression and functions in human colorectal cancer (CRC) have been rarely explored. The present study verified the high expression of GOLM1 within CRC tissues and cell lines. GOLM1 was positively correlated with vascular invasion, TNM stage, and lymph node metastasis among CRC cases. In vitro experiments showed that GOLM1 downregulation inhibited the growth, migration, and invasion of Caco-2 and HCT116 cells, while the overexpression of GOLM1 facilitated the growth, migration, and invasion of SW480 cells. In vivo experiments revealed that the knockdown of GOLM1 reduced the growth of nude mouse xenografts and lung metastasis of HCT116 cells. Furthermore, GOLM1 was found to be a motivator for the epithelial-mesenchymal transition (EMT) phenotype and the AKT/GSK3β pathway in CRC cells. Finally, MK2206, an AKT inhibitor, could markedly reverse GOLM1-elicited proliferation, migration, invasion, and EMT phenotype by inhibiting the AKT/GSK3β pathway. Collectively, our data indicate that GOLM1 facilitates human CRC progression and metastasis via activating the AKT/GSK3β/EMT axis. Most importantly, our study makes substantial support for the clinical translation of GOLM1 in CRC target therapy.