PRMT7 (Protein Arginine Methyltransferase 7)

Enhanced Prmt7-dependent tumor growth was not observed in immunodeficient mice, implicating Prmt7 in immune evasion. This study underscores the utility of CRISPR screens for high-throughput functional follow-up of GWAS findings and identifies PRMT7 inhibition as a promising therapeutic strategy.

Consistent with these findings, clinical analysis revealed significant co-upregulation of both PRMT7 and SOX9 in NSCLC specimens relative to adjacent normal tissues, with elevated levels of either protein correlating with diminished patient survival. Collectively, our findings establish PRMT7 as a key regulator of SOX9 stability and function, thereby highlighting the PRMT7-SOX9 axis as a promising therapeutic target in NSCLC.

Consistently, in human brain tissue, JCV-infected glial cells displayed maintenance of a diploid chromosomal complement, likely through G2 arrest. The precise mechanism of this, however, remains to be elucidated.

Furthermore, PRMT7 regulated the functions of Yin Yang 1 (YY1), tumor protein p53 (TP53), cyclin D2 (CCND2), CDK6 and retinoblastoma 1 (RB1) in PCa. PRMT7 may promote proliferation, migration and metastasis in PCa cells by regulating the activity of YY1, TP53, CCND2, CDK6 and RB1 in the cell cycle signaling pathway.

Conversely, PRMT7 overexpression or treatment with the PRMT7-inducing drug bindarit restores EC function, suppresses ER stress and enhances revascularization and cardiac repair after MI. These findings establish endothelial PRMT7 as a critical regulator of EC survival and function, highlighting its potential as a therapeutic target to mitigate ER stress and improve post-MI cardiac recovery.

By concurrently targeting MYC and multiple PRMTs, 3-alkenylindol-2-one overcomes the limitations of single-target therapies, offering a novel strategy to suppress proliferation and promote antitumor immunity in AML. These findings establish PRMTs as critical downstream mediators of MYC-driven leukemogenesis and position 3-alkenylindol-2-one as a promising clinical candidate for AML treatment, providing a mechanism-based approach to target MYC-driven leukemia through its downstream epigenetic regulators.

We developed a PRMTs-related prognostic model for assessing prognosis and immunotherapy responses in LUAD. This model was vital for developing more personalized and effective treatment plans for LUAD patients.

More importantly, A33 exhibited low toxicity and effectively suppressed PCa tumor growth in the DU-145 xenograft tumor model. Collectively, this study provides a novel potent PRMT7 inhibitor for further anti-PCa drug discovery.

This study systematically reveals the molecular mechanisms of smoking-linked NSCLC through multidimensional bioinformatics analysis, highlighting the key roles of SLDCGs in immune evasion. The discovery of HLA-J and PRMT7 provides new theoretical foundations for targeted immunotherapy, with significant potential for early diagnosis and personalized treatment of smoking-induced NSCLC. Future research should focus on validating these genes in clinical samples and exploring their potential in immunotherapy.

We also find that SGC3027 specifically activates ATM kinase and its downstream cell cycle checkpoint kinases to enhance radiobiological response in NSCLC. These findings underscore the promising therapeutic potential of PRMT7 inhibitors as well as combining PRMT7 inhibition with irradiation exposure for effective NSCLC therapies.

Moreover, we also focus on recent progress in the design and development of modulators targeting PRMT7, including isoform-selective and non-selective PRMT7 inhibitors, and the dual-target inhibitors based on PRMT7, from the perspectives of rational design, pharmacodynamics, pharmacokinetics, and the clinical status of these modulators. Finally, we also provided the challenges and prospective directions for PRMT7 targeting drug discovery in cancer therapy.

METTL3/IGF2BP1 facilitates the progression of TNBC by mediating m6A methylation modification of PRMT7.