Arginine methyltransferase PRMT3 promote tumorigenesis through regulating c-MYC stabilization in colorectal cancer

Gene. 2021 Jul 30:791:145718. doi: 10.1016/j.gene.2021.145718. Epub 2021 May 13.

Abstract

The incidence rates of colorectal cancer have been increasing in the last decades, yet the overall survival rate is still not ideal. There is a need to further investigate detailed mechanism for colorectal cancer tumorigenesis. The biological function of protein arginine methyltransferases 3 (PRMT3) is seldom studied in tumorigenesis. Here, we attempted to elucidate the link between PRMT3 and tumorigenesis in colorectal cancer. Results revealed that PRMT3 was upregulated in colorectal cancer. Besides, PRMT3 overexpression promoted colorectal cancer cell proliferation, migration, and invasion. Regarding mechanism for colorectal cancer tumorigenesis, PRMT3 stabilized C-MYC and the pro-tumorigenesis function of PRMT3 was dependent on C-MYC. Clinically, these findings might provide a novel therapeutical treatment strategy for colorectal cancer.

Keywords: C-MYC; Colorectal cancer; PRMT3.

MeSH terms

  • Carcinogenesis / genetics
  • Cell Line, Tumor
  • Cell Movement / genetics
  • Cell Proliferation / genetics
  • Cell Transformation, Neoplastic / genetics
  • Colorectal Neoplasms / metabolism*
  • Humans
  • Intracellular Signaling Peptides and Proteins / metabolism
  • Intracellular Signaling Peptides and Proteins / physiology
  • Methylation
  • Neoplasm Invasiveness / genetics
  • Protein-Arginine N-Methyltransferases / metabolism*
  • Protein-Arginine N-Methyltransferases / physiology
  • Proto-Oncogene Proteins c-myc / genetics
  • Proto-Oncogene Proteins c-myc / metabolism
  • Ribosomal Proteins / metabolism

Substances

  • Intracellular Signaling Peptides and Proteins
  • MYC protein, human
  • Proto-Oncogene Proteins c-myc
  • Ribosomal Proteins
  • PRMT2 protein, human
  • PRMT3 protein, human
  • Protein-Arginine N-Methyltransferases