2. Academic Validation
  3. PRMT3 promotes tumorigenesis by methylating and stabilizing HIF1α in colorectal cancer

PRMT3 promotes tumorigenesis by methylating and stabilizing HIF1α in colorectal cancer

  • Cell Death Dis. 2021 Nov 9;12(11):1066. doi: 10.1038/s41419-021-04352-w.
Xin Zhang  # 1,  Kexin Wang  # 1,  Xingbo Feng 2,  Jian Wang 3,  Yali Chu 1,  Chunmeng Jia 1,  Qingsi He 1,  Cheng Chen 4
Affiliations

Affiliations

  • 1 Department of General Surgery, Qilu Hospital of Shandong University, 107 West Wenhua Road, Jinan, China.
  • 2 Department of General Surgery, Central Hospital of Zaozhuang Coal Mining Group, Shandong Province, Zaozhuang, China.
  • 3 Department of General Surgery, Jinan integrative medicine hospital, 8 east Wenyuan street, Jian, China.
  • 4 Department of General Surgery, Qilu Hospital of Shandong University, 107 West Wenhua Road, Jinan, China. cc_089@126.com.
  • # Contributed equally.
PMID: 34753906 DOI: 10.1038/s41419-021-04352-w
Abstract

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.

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