The nucleolar protein NIFK accelerates the progression of colorectal cancer via activating MYC pathway

This study aimed to explore the function of NIFK on colorectal Cancer (CRC) and its associated molecular mechanisms. NIFK was upregulated in CRC tissues and cells. NIFK silencing resulted in reduced cell growth and metastasis, as well as in promoted Apoptosis in CRC cells. Moreover, NIFK silencing was also confirmed to inhibit lipid accumulation and decrease fatty acid synthesis via downregulating lipogenic Enzymes in CRC cells. Gene Set Enrichment Analysis and western blot co-verified that NIFK silencing inhibited MYC pathway in CRC cells. In addition, we also revealed that NIFK silencing function on cell growth, Apoptosis, metastasis and fatty acid metabolism in CRC might be cancelled after c-Myc overexpression. Silencing NIFK could inhibit cell growth and metastasis, and promoted Apoptosis, as well as regulated fatty acid metabolism by inhibiting MYC pathway in CRC.

CRC; MYC; NIFK; fatty acid metabolism.