PRMT1 (Protein Arginine Methyltransferase 1)

Importantly, dual inhibition of PRMT1 and PRMT5 synergistically sensitizes tumors to PARP inhibitors. Collectively, our findings provide strong rationale for the clinical development of PRMT and PARP inhibitor combinations in HR-proficient ovarian and breast cancers.

Rescue experiments demonstrated that re-expression of Sh2b1-T1, but not Sh2b1-T2, reversed the impairment of osteoblast differentiation triggered by Ddx17 knockdown. Taken together, these findings underscore the critical role of the Prmt1-Ddx17-Sh2b1 axis in regulating osteoblast differentiation and suggest this axis as a promising therapeutic target for osteoporosis.

We conclude that SKLB06489 is a potent type Ⅰ PRMTs inhibitor with great therapeutic potential and is expected to overcome the TNBC treatment bottleneck. The discovery of SKLB06489-regulated cholesterol homeostasis provides a novel perspective on the biological function of type Ⅰ PRMTs, particularly their role in regulating metabolic pathway.

Finally, inhibition of the ATR regulators PRMT1 or PRMT5 synergizes with PARG inhibition, implicating replication-associated BER/SSBR and PARylation in the activation of the PRMT1/PRMT5/ATR axis. This study highlights the role of BER/SSBR in protecting the cell during S-phase to suppress PARylation-induced checkpoint activation, which may suggest a potential intervention strategy for PARG inhibitor-resistant tumors.

Notably, PRMT1 rs975484 was also correlated with hemoglobin (HGB) level, and may serve as an independent favorable prognostic factor in DLBCL. Our findings suggest that SNPs involved in cGAS-STING-mediated type I interferon pathway may influence DLBCL susceptibility, treatment response, and prognosis, highlighting their potential as biomarkers for risk stratification and for guiding individualized disease monitoring.

Collectively, these findings unveil a previously unrecognized signaling pathway that coordinately regulates DNA repair fidelity and invasive potential in GBM. Our work proposes the FOSL1‑PRMT1‑CAPS axis as a promising therapeutic target for overcoming radioresistance and improving treatment outcomes in GBM patients.

The DNM exhibits a specific affinity toward CD44-overexpressing tumor cells, enabling the effective delivery of the loaded cisplatin (CDDP) to the tumor cells...This temporally programmed release enables the reversal of cancer stemness before chemotherapy initiation, resulting in a substantial improvement in CDDP chemosensitivity and a significant increase in the median survival of tumor-bearing mice from 27 to over 56 d with DNM assistance. This study highlights the promising potential of this DNA nanotechnology-empowered therapy in addressing chemoresistance in malignant tumors.

PRMT1 drives OSCC aggressiveness by methylating and activating STAT3. This axis promotes chemoresistance and oncogenic phenotypes primarily by suppressing ferroptosis through STAT3-mediated transcriptional upregulation of GPX4. Targeting PRMT1 represents a promising strategy to overcome chemoresistance and inhibit progression in OSCC.

This review offers new perspectives on PRMT1-related disease mechanisms and lays a theoretical foundation for the development of targeted therapies. Ultimately, this review aims to contribute to the progression of precision medicine and the enhancement of global health outcomes.

WTAP regulated the m6A modification and mRNA stability of PRMT1. The WTAP/PRMT1 signaling axis modulated cuproptosis, thereby influencing ATC progression. These findings highlighted the potential of targeting the WTAP/PRMT1 pathway as a therapeutic strategy for ATC.

Treatment with the Type I PRMT inhibitor GSK3368715 resulted in a dose-dependent reduction in cell survival across a panel of MM cell lines...This was supported by Reverse Phase Protein Array (RPPA) analyses, which revealed a significant reduction in levels of proteins associated with cell cycle regulation and DDR pathways. Overall, our findings indicate that MM cells critically depend on PRMT1 for survival, highlighting the therapeutic potential of PRMT1 inhibition in treating MM.