Cancer synthetic vulnerabilities to protein arginine methyltransferase inhibitors

Protein arginine methylation is an abundant post-translational modification involved in the modulation of essential cellular processes ranging from transcription, post-transcriptional RNA metabolism, and propagation of signaling cascades to the regulation of the DNA damage response. Excitingly for the field, in the past few years there have been remarkable advances in the development of molecular tools and clinical compounds able to selectively and potently inhibit protein arginine methyltransferase (PRMT) functions. In this review, we first discuss how the somatic mutations that confer advantages to cancer cells are often associated with vulnerabilities that can be exploited by PRMTs' inhibition. In a second part, we discuss strategies to uncover synthetic lethal combinations between existing therapies and PRMT inhibitors.

Automated summary

Protein arginine methylation plays a crucial role in regulating cellular processes, and significant progress has been made in the development of molecular tools and clinical compounds to inhibit PRMT functions. Studies have shown that somatic mutations in cancer cells can create vulnerabilities that can be exploited through PRMT inhibition. Additionally, research has identified synthetic lethal combinations between existing therapies and PRMT inhibitors.