Overexpression of golgi membrane protein 1 promotes non-small-cell carcinoma aggressiveness by regulating the matrix metallopeptidase 13.

Abstract

Non-small-cell carcinoma (NSCLC) is one of the most lethal malignancies of lung cancers and its prognosis remains dismal due to the paucity of effective therapeutic targets. Recent reports show that Golgi membrane protein 1 (GOLM1) is highly expressed in a variety of tumor cells, functions as a negative regulator of T cells and then promotes tumor progression. However, its expression and role in NSCLC remain unclear. Herein, we showed that GOLM1 was markedly up-regulated in NSCLC cell lines and clinical tissues. Clinically, NSCLC patients with high expression of GOLM1 had shorter overall survival (OS) and high GOLM1 expression in tumor samples was significantly related to malignant phenotype, such as lymph node metastasis and high tumor stage. Ectopic expression of GOLM1 in NSCLC cells induced epithelial-to-mesenchymal transition (EMT) and promoted proliferation, migration, and invasion of NSCLC cells in vitro. Furthermore, GOLM1 overexpressing significantly promoted the tumorigenicity of NSCLC cells in vivo whereas silencing endogenous GOLM1 caused an opposite outcome. Moreover, we demonstrated that GOLM1 enhanced NSCLC aggressiveness by activating matrix metalloproteinase-13 (MMP13) signaling. Together, our results provided new evidence that GOLM1 overexpression promoted the progression of NSCLC and might represent a novel therapeutic target for its treatment.