Nop2, also known as NSUN1, is an S-adenosyl-L-methionine-dependent methyltransferase belonging to the NOL1/NOP2/SUN domain (NSUN) family. It is crucial for catalyzing the post-transcriptional modification of RNA through 5-methylcytosine (m5C) [2,4]. This m5C modification is involved in multiple biological processes, including ribosome biogenesis, cell cycle regulation, and cell proliferation [2,5].

In hepatocellular carcinoma (HCC), Nop2 knockout in combination with sorafenib enhanced sorafenib sensitivity and inhibited tumor growth. Mechanistically, NOP2 regulates c-Myc expression via m5C-modification to promote glycolysis, and m5C methylation of c-Myc mRNA leads to its degradation in an EIF3A-dependent manner. Also, NOP2 increases the expression of glycolytic genes [1]. In clear cell renal cell carcinoma (ccRCC), loss-of-function assays showed that NOP2 affects cell proliferation, migration, and invasion. It stimulates m5C modification of APOL1 mRNA, which is then stabilized by YBX1, and this affects ccRCC progression via the PI3K-Akt signaling pathway [3].

In conclusion, Nop2 plays significant roles in regulating biological processes through m5C-mediated RNA modification. Gene knockout models, especially in the context of cancers like HCC and ccRCC, have revealed its importance in tumor progression, metabolism reprogramming, and potential as a therapeutic target. These findings contribute to a better understanding of disease mechanisms and may offer new strategies for treatment.