FABP7 promotes cell proliferation and survival in colon cancer through MEK/ERK signaling pathway.

Abstract

Colon cancer (CC), one of the most frequently diagnosed malignancies deriving from the digestive system, has greatly threatened human health and life. Fatty acid binding protein 7 (FABP7), an intracellular protein with the tissue-specific expression pattern, has been reported to be implicated in diverse types of human tumors. However, the biological role of FABP7 in CC is still poorly understood. The current study aimed to investigate the role of FABP7 in CC and illuminate the potential molecular mechanisms. In this present study, we found that FABP7 was highly expressed in CC tissues and cell lines, suggesting the possible involvement of FABP7 in CC tumorigenesis. Moreover, functional investigations showed that FABP7-overexpression promoted CC cell proliferation, colony formation, cell cycle progression and inhibited cell apoptosis; on the contrary, FABP7 knockdown produced an inhibitory effects on CC cell proliferation and survival. Notably, FABP7 knockdown inhibited colon tumor growth in vivo. In addition, mechanistic investigations demonstrated that FABP7 exerted its promoting effects on CC cell proliferation and survival through activation of the MEK/ERK signaling pathway. Collectively, our data indicate that FABP7 may be used as a novel diagnostic bio-marker and a potential therapeutic target for CC.