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

Abstract

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.

Nucleolar protein interacting with the FHA domain of MKI67 may be an important factor in promoting the development of colorectal cancer: a comprehensive study integrating bulk RNA-seq, scRNA-seq, protein immunohistochemistry and CRISPR

“…Although the mRNA expression pro les of these CRC tissue come from a wide range of sources and may have many obvious heterogeneities due to the inconsistencies in the technical level and standards of individual studies, the comprehensive analysis described above demonstrates that it is possible to pool and analyse these data sets without signi cantly affecting the accuracy and reliability of the results. This is supported by previous studies that found high NIFK expression in CRC based on only a small RNA sequencing dataset (14,15). And the same view was further argued by qualitative and quantitative immunohistochemical analysis of 266 CRC tissue with corresponding paracancerous tissue within this study.…”

“…In vitro experiments have shown that silencing NIFK inhibits the proliferation of osteosarcoma cells through p53-dependent G1 phase arrest (13). As for colorectal cancer, previous studies have shown that NIFK is signi cantly overexpressed in CRC and associated with immune in ltration (14,15). However, these studies have some limitations.…”