本研究旨在探讨NIFK在结直肠癌（CRC）中的作用及其相关分子机制。 NIFK 在 CRC 组织和细胞中表达上调。 NIFK 沉默导致细胞生长和转移减少，并促进 CRC 细胞凋亡。此外，NIFK 沉默还被证实可以通过下调 CRC 细胞中的脂肪生成酶来抑制脂质积累并减少脂肪酸合成。基因集富集分析和蛋白质印迹共同验证 NIFK 沉默抑制 CRC 细胞中的 MYC 通路。此外，我们还发现，c-MYC过表达后，NIFK沉默对CRC细胞生长、凋亡、转移和脂肪酸代谢的作用可能被取消。沉默 NIFK 可以抑制细胞生长和转移，促进细胞凋亡，并通过抑制 CRC 中的 MYC 通路来调节脂肪酸代谢。© 作者 2023。由牛津大学出版社代表日本生物科学、生物技术学会出版，和农业化学。

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.© The Author(s) 2023. Published by Oxford University Press on behalf of Japan Society for Bioscience, Biotechnology, and Agrochemistry.