The role of protein arginine methyltransferases in pathogenesis and treatment of digestive system carcinoma.
Bin WangDong DingXiao-An ZhangJunxi ZhangHuanhuan ZhangXinxin LiuHui ChangZhan GaoZengli YuPublished in: Molecular cancer therapeutics (2023)
Post-translational modification of proteins increases their diversity and maintains the stability of the intracellular environment. Protein arginine methyltransferases (PRMTs) are an important family of epigenetic modification enzymes, which play a critical role in post-translational modification. In recent years, with the in-depth study of the role of epigenetics, the structure and function of PRMTs have been gradually understood. PRMT enzymatic activity is related to a variety of cellular processes in digestive system malignancies, such as inflammation and immune response, activation of cell cycle and proliferation, inhibition of apoptosis, DNA damage repair, epithelial-mesenchymal transition (EMT). A variety of chemical tools are developed to inhibit PRMT activity, which have been verified by tumor models and clinical trials. This review summarizes the structure and functions of PRMTs as a prelude to our further studies on their role in tumors. The involvement of different PRMTs in the pathogenesis of gastrointestinal tumors is then reviewed. In addition, the application of PRMT inhibitors as therapeutic agents for digestive system cancers is highlighted. In conclusion, PRMTs play an important role in the pathogenesis of gastrointestinal tumors, and their prognostic and therapeutic potential warrants further investigation.
Keyphrases
- cell cycle
- epithelial mesenchymal transition
- oxidative stress
- dna damage
- immune response
- clinical trial
- amino acid
- nitric oxide
- signaling pathway
- cell proliferation
- transforming growth factor
- endoplasmic reticulum stress
- hydrogen peroxide
- dna repair
- binding protein
- optical coherence tomography
- randomized controlled trial
- protein protein
- dendritic cells
- young adults
- small molecule
- reactive oxygen species
- inflammatory response
- combination therapy
- toll like receptor