The metabolic enzyme methionine adenosyltransferase 2α (MAT2A) was identified as a synthetic lethal target in MTAP-deleted cancers. The study was conducted to report the characterization of potent MAT2A inhibitors that substantially reduce levels of S-adenosylmethionine (SAM) and demonstrate antiproliferative activity in MTAP-deleted cancer cells and tumors. MAT2Ai reduce PRMT5 activity affecting mRNA splicing and inducing DNA damage. The methylthioadenosine phosphorylase ( MTAP) gene is located adjacent to the cyclin-dependent kinase inhibitor 2A ( CDKN2A) tumor-suppressor gene and is co-deleted with CDKN2A in approximately 15% of all cancers. show that DNA damage and mitotic defects ensue upon MAT2A inhibition in HCT116 MTAP −/− cells, providing a rationale for combining the MAT2A clinical candidate AG-270 with antimitotic taxanes. As a conclusion it is observed that using RNA sequencing and proteomics, researchers demonstrate that MAT2A inhibition is mechanistically linked to reduced protein arginine methyltransferase 5 (PRMT5) activity and splicing perturbations. AGI-24152 and AG-270 reduce proliferation of cancer cells and tumors that lack MTAP. Antiproliferative effects of AG-270 are synergistic with taxanes in vitro and in vivo.
Exosomes: Multiple-targeted multifunctional biological nanoparticles in the diagnosis, drug delivery, and imaging of cancer cells.
June 29, 2020
Phase I/II study of erlotinib to determine the optimal dose in patients with non-small cell lung cancer harboring only EGFR mutations.
April 22, 2020
Gene signatures based on therapy responsiveness provide guidance for combined radiotherapy and chemotherapy for lower grade glioma.
March 12, 2020
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