Overexpression of family with sequence similarity 134, member B (FAM134B) in colon cancers and its tumor suppressive properties in vitro.

This study aims to investigate the overexpression-induced properties of tumor suppressor (family with sequence similarity 134, member B) in colon cancer, examine the potential gene regulators of expression and its impact on mitochondrial function. was overexpressed in colon cancer and non-neoplastic colonic epithelial cells. Various cell-based assays including apoptosis, cell cycle, cell proliferation, clonogenic, extracellular flux and wound healing assays were performed. Western blot analysis was used to confirm and identify potential interacting partners of . Immunohistochemistry and qPCR were employed to determine the expressions of MIF and , respectively, on 63 patients with colorectal carcinoma. Results showed that is involved in the cell cycle and mitochondrial function of colon cancer. Overexpression of was coupled with increased expression levels of APC, p53, and MIF. Increased expression of both APC and p53 further validates the potential role of tumor suppressor in regulating cancer progression through the WNT/ß-catenin signaling pathway. In approximately 70% of the patients with colorectal cancer, downregulation was correlated with MIF protein overexpression while the remaining 30% showed concurrent expression of and MIF ( = .045). High expression of MIF coupled with low expression of is associated with microsatellite instability status in colorectal carcinomas ( = .049). may exert its tumor suppressive function through affecting cell cycle, mitochondrial function via potentially interacting with MIF and p53.