Nat10-mediated ac4C modification sustains macrophage proliferation and mitigates colitis progression via Mcm2 stabilization.

Targeting the AKT2-NAMPT phosphorylation axis prevents macrophage senescence to enhance bactericidal activity in septic immunosuppression.

A dual-layer regulatory mechanism in which DDX6 controls NAMPT abundance, whereas AKT2 dictates its activity drives senescence during immune tolerance is identified, identifying AKT2-NAMPT as a potential therapeutic axis to restore immune competence in sepsis.

The RNA modification N6-methyladenosine restrains SIRPα to license myeloid efferocytosis in atherosclerosis

USP36-mediated stabilization of NAT10 promotes osteosarcoma progression via ac4C-dependent KIF23 mRNA stabilization.

Osteosarcoma is an aggressive bone malignancy with a propensity for pulmonary metastasis, yet the molecular mechanisms linking protein homeostasis to epitranscriptomic regulation remain incompletely understood. Here, integrated transcriptomic, survival, protein-interaction, and CRISPR dependency analyses identified the...

Macrophage PABPC4‐SPP1 Axis Orchestrates Immunosuppression in Colorectal Cancer

It is identified that PABPC4, a member of PABPs, is upregulated during colorectal cancer progression and associated with poor prognosis, and a previously undiscovered PABPC4‐SPP1 axis in macrophages is revealed, which induces tumor‐promoting macrophages and CD8+ T cell dysfunction, thereby facilitating tumor progressio...

NAT10 promotes prostate cancer progression by acetylating mRNA of MARK2 and activating mTOR/HIF-1α/C-Myc pathway to enhance glycolytic reprogramming.

Mechanistic investigations demonstrated that NAT10 elevates MARK2 expression, activating the mTOR/HIF-1α/C-Myc signaling cascade, thereby promoting aerobic glycolysis in PCa cells, suggesting that targeting ac4C mRNA modifications may provide a novel therapeutic strategy for managing prostate cancer.

MCM10 Modulates Lipid Metabolic Reprogramming via the USP7-FASN Axis to Accelerate Renal Cell Carcinoma Progression.

Metabolic reprogramming, particularly dysregulated lipid metabolism, is a hallmark of clear cell renal cell carcinoma (ccRCC) progression. However, the upstream regulators responsible for lipid metabolic rewiring remain largely unknown. Here, we integrated single-cell RNA sequencing, spatial transcriptomics, and functi...