PRMT1 (Protein Arginine Methyltransferase 1)

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.

Co-culture assays confirmed that GV1001 blunts microglial neurotoxicity and facilitates remyelination during inflammation. Collectively, the data indicate that GV1001 modulates microglial activity to attenuate neuroinflammation and foster spinal cord repair, underscoring its promise as a multitarget therapy for inflammatory demyelinating diseases such as multiple sclerosis.

Notably, combination therapy using PRMT5 inhibitor GSK3326595 along with cisplatin and etoposide significantly delayed the recurrence of SCLC. Our findings reveal the promoting effect of post-chemotherapy inflammation on tumor recurrence from an epigenetic perspective and provide a potential therapeutic strategy for SCLC treatment.

TI reversed the resistance of SW620/AD300 and KBV200 cells to doxorubicin (DOX) and paclitaxel (PAC) by downregulating ABCB1 expression and reducing ABCB1 drug transport function. Additionally, TI demonstrated resistance reversal to PAC in xenograft models without detectable toxicities. This study establishes TI's MDR reversal effect in ABCB1-mediated MDR human cancer cells through inhibition of PRMT1-mediated aDMA of EGFR, suggesting TI's potential as an MDR modulator for improving chemotherapy outcomes.

Genetic knockdown or pharmacological inhibition of ATG4B in AML cells restores DNA repair capacity, activates the cell-cycle checkpoint kinase CHEK1/CHK1, attenuates malignant progression, and ultimately delays leukemia progression. These findings reveal an autophagy-independent role for nuclear ATG4B that links metabolic stress to the suppression of DNA repair and identify ATG4B as a potential therapeutic target in AML.

Meanwhile, compound 30t displayed good pharmacokinetic properties and favorable antitumor activity in vivo. Collectively, this study provides a novel compound for further development of anticancer drugs.

Additionally, high PRMT1 expression contributed to increased resistance to docetaxel in TNBC...PRMT1 drives lung metastasis and chemoresistance in TNBC through PARP1 methylation and P65 activation. These findings position PRMT1 as a promising biomarker and therapeutic target to overcome resistance and limit metastatic progression in TNBC.

Furthermore, we found that PRMT1 knockdown in GC affects the STAT pathway in TAMs, inducing changes in their polarization and promoting GC apoptosis by enhancing IFN-β secretion through the cGAS/STING pathway. In summary, our findings revealed that PRMT1 knockdown inhibits the cGAS/STING pathway in GC, which produces type I IFNs to promote the polarization of M1-like macrophages in the tumor microenvironment.