Tumor suppressor Parkin induces p53-mediated cell cycle arrest in human lung and colorectal cancer cells

BMB Rep. 2023 Oct;56(10):557-562. doi: 10.5483/BMBRep.2023-0134.

Abstract

Dysregulation of the E3 ubiquitin ligase Parkin has been linked to various human cancers, indicating that Parkin is a tumor suppressor protein. However, the mechanisms of action of Parkin remain unclear to date. Thus, we aimed to elucidate the mechanisms of action of Parkin as a tumor suppressor in human lung and colorectal cancer cells. Results showed that Parkin overexpression reduced the viability of A549 human lung cancer cells by inducing G2/M cell cycle arrest. In addition, Parkin caused DNA damage and ATM (Ataxia telangiectasia mutated) activation, which subsequently led to p53 activation. It also induced the p53-mediated upregulation of p21 and downregulation of cyclin B1. Moreover, Parkin suppressed the proliferation of HCT-15 human colorectal cancer cells by a mechanism similar to that in A549 lung cancer cells. Taken together, our results suggest that the tumor-suppressive effects of Parkin on lung and colorectal cancer cells are mediated by DNA damage/p53 activation/cyclin B1 reduction/cell cycle arrest. [BMB Reports 2023; 56(10): 557-562].

Publication types

  • News

MeSH terms

  • Apoptosis
  • Cell Cycle
  • Cell Cycle Checkpoints
  • Cell Line, Tumor
  • Colorectal Neoplasms* / genetics
  • Cyclin B1 / genetics
  • Cyclin B1 / metabolism
  • Humans
  • Lung / metabolism
  • Lung Neoplasms* / pathology
  • Tumor Suppressor Protein p53 / genetics
  • Tumor Suppressor Protein p53 / metabolism
  • Ubiquitin-Protein Ligases / genetics
  • Ubiquitin-Protein Ligases / metabolism

Substances

  • Cyclin B1
  • Tumor Suppressor Protein p53
  • Ubiquitin-Protein Ligases
  • parkin protein
  • TP53 protein, human