NOP2 (NOP2 Nucleolar Protein)

Both HCC tissues and cell models consistently demonstrated elevated NSNU5 mRNA and protein expression. Genetic inhibition of the m5c methyltransferase NSUN5 suppresses HCC cell growth, reduces invasiveness and migration, and induces apoptosis.

NSUN6 regulated the m5C methylation modification of PKP2 to stabilize its expression, thereby driving the malignant progression of OS cells, providing a promising targeted therapeutic strategy for OS.

Depletion of NOP2 selectively inhibited MYC liver cancer cell proliferation and in vivo tumor growth. Thus, methionine catabolism is critical for MYC-driven liver tumorigenesis and the rRNA methyltransferase NOP2 may serve as a new therapeutic target in liver cancer.

In conclusion, NSUN7 promotes pyroptosis of lung epithelial cells in sepsis-induced ALI by stabilizing TRAF6 in a m5C-dependent manner. These findings suggest that NSUN7 may be a promising therapeutic target for sepsis-induced ALI.

NSUN6 deficiency drives immune suppression through the m5C-KDM5A-CCL2 axis in PDAC. Targeting the NSUN6-CCL2 axis represents a promising strategy to sensitise PDAC to ICB therapy.

NSUN2-mediated m5C modification of EPYC contributed to GC cell growth and metastasis, which provided a novel regulatory axis for understanding the pathogenesis of GC.

In summary, this study reveals that NOP2 facilitates larynx cancer progression by enhancing glycolysis through m5C-mediated stabilization of TPI1 mRNA. Our findings uncover the NOP2/m5C/TPI1 axis as a novel therapeutic target and provide new insights into RNA methylation-driven metabolic reprogramming in larynx cancer.

NSUN2 is the most studied NSUN family gene, which exhibits cancer promoting effects in various cancers such as lung cancer, liver cancer, and colorectal cancer. This review provides an overview of the roles of NSUN family genes in methylation, diagnostic value, inflammatory diseases, cancer, and other diseases.

Conversely, NSUN2 overexpression conferred ferroptosis resistance, reducing iron accumulation and restoring GPX4 expression even under erastin treatment...Notably, treatment with an autophagy inhibitor (3-MA) or a ferroptosis inhibitor (Fer-1) partially restored tumor growth in NSUN2-knockdown cells, validating the critical role of autophagy and ferroptosis in NSUN2-mediated OSCC progression. These findings identify the NSUN2-YBX1-SQSTM1/P62 axis as a key regulator of autophagy-dependent ferroptosis in OSCC, highlighting NSUN2 as a promising epitranscriptomic target to enhance ferroptosis induction for OSCC therapy.

Finally, we discuss the translational implications of targeting NSUN-mediated m5C pathways, highlighting small-molecule inhibitors designed against NSUN substrate specificity, combinatorial strategies with conventional chemotherapy or immunotherapy, and the promise of epitranscriptomic diagnostics and prognostic based on NSUN expression signatures. By positioning NSUN proteins as integral nodes in the RNA epigenomic network, this synthesis not only deepens our understanding of cancer pathogenesis but also identifies novel epitranscriptomic targets for precision oncology.

Collectively, our data suggest that erianin serves as an inhibitor of vasculogenic mimicry. Our results unveil a novel therapeutic strategy for combating malignant progression by fine-tuning m5C modification with a natural product.

Additionally, this process involves the assistance and balance of the reader YBX1 and the eraser TET2. NSUN2 methylates SOCS3 mRNA to inhibit its stability and nuclear export, which consequently promotes macrophage polarization to M2.