PRMT3 promotes tumorigenesis by methylating and stabilizing HIF1α in colorectal cancer.
Xin ZhangKexin WangXingbo FengJian WangYali ChuChunmeng JiaQingsi HeCheng ChenPublished in: Cell death & disease (2021)
Abnormal angiogenesis occurs during the growth of solid tumors resulting in increased vascular permeability to fluids and metastatic cancer cells. Anti-angiogenesis therapy for solid tumors is effective in the treatment of cancer patients. However, the efficacy of anti-angiogenesis therapy is limited by drug resistance. The findings of the current study showed that HIF1α R282 is methylated by PRMT3, which is necessary for its stabilization and oncogene function. Analysis showed that PRMT3-mediated tumorigenesis is HIF1α methylation-dependent. A novel therapeutic molecule (MPG-peptide) was used to inhibit HIF1α expression. These findings provided information on PRMT3 signaling pathway and HIF1/VEGFA signaling pathway and offer a novel therapeutic strategy for colorectal cancer, mainly for treatment of anti-angiogenesis resistance patients.
Keyphrases
- endothelial cells
- signaling pathway
- vascular endothelial growth factor
- end stage renal disease
- squamous cell carcinoma
- small cell lung cancer
- poor prognosis
- newly diagnosed
- wound healing
- ejection fraction
- chronic kidney disease
- healthcare
- gene expression
- prognostic factors
- combination therapy
- peritoneal dialysis
- bone marrow
- health information
- social media