GOLM1 silencing inhibits the proliferation and motility of human glioblastoma cells via the Wnt/β-catenin signaling pathway

Golgi membrane protein 1 (GOLM1) is a type II transmembrane protein located in the cis- and medial-Golgi. Due to its function as an oncogene and proprotein convertase (PC) consensus site, GOLM1 will play a vital role in gene-targeted therapies and serve as a candidate tumor biomarker. However, few studies have explored its correlation with glioblastoma (GBM) progression. In this study, we detected the overexpression of the GOLM1 mRNA and protein in clinical GBM samples. The level of secreted GOLM1 in the serum from patients with GBM was also abnormally elevated, as determined by an Elisa. Then we utilized small interfering RNAs (siRNAs) to silence GOLM1 expression in GBM U87 and U251 cells. After silencing GOLM1 expression, the proliferation of cells decreased, the cell cycle was arrested in G1/S phase, and tumor cell motility was also inhibited. Moreover, the levels of proliferation-associated proteins and epithelial-mesenchymal transition (EMT)-related markers were also altered. Additionally, the Wnt/beta-catenin signaling pathway was significantly suppressed, particularly the nuclear translocation of beta-catenin. Knockdown of GOLM1 also inhibits xenograft tumor growth in nude mouse models.GOLM1 acts as a critical oncogene in GBM by promoting cell proliferation, migration and invasion. Its mechanism may be related to the Wnt/beta-catenin signaling pathway. GOLM1 also exhibits great potential as a biomarker for GBM.