TP53I11 suppresses epithelial-mesenchymal transition and metastasis of breast cancer cells

BMB Rep. 2019 Jun;52(6):379-384. doi: 10.5483/BMBRep.2019.52.6.173.

Abstract

Epithelial-mesenchymal transition (EMT) is widely-considered to be a modulating factor of anoikis and cancer metastasis. We found that, in MDA-MB-231 cells, TP53I11 (tumor protein P53 inducible protein 11) suppressed EMT and migration in vitro, and inhibited metastasis in vivo. Our findings showed that hypoxic treatment upregulated the expression of HIF1α, but reduced TP53I11 protein levels and TP53I11 overexpression reduced HIF1α expression under normal culture and hypoxicconditions, and in xenografts of MDA-MB-231 cells. Considering HIF1α is a master regulator of the hypoxic response and that hypoxia is a crucial trigger of cancer metastasis, our study suggests that TP53I11 may suppress EMT and metastasis by reducing HIF1α protein levels in breast cancer cells. [BMB Reports 2019; 52(6): 379-384].

MeSH terms

  • Animals
  • Breast Neoplasms / metabolism*
  • Breast Neoplasms / pathology
  • Cell Hypoxia / physiology
  • Cell Line, Tumor
  • Cell Movement / physiology
  • Cell Proliferation / physiology
  • Epithelial-Mesenchymal Transition
  • Female
  • Heterografts
  • Humans
  • Hypoxia-Inducible Factor 1, alpha Subunit / metabolism
  • Mice
  • Mice, Nude
  • Neoplasm Metastasis
  • Neoplasm Proteins / metabolism*

Substances

  • HIF1A protein, human
  • Hypoxia-Inducible Factor 1, alpha Subunit
  • Neoplasm Proteins
  • TP53I11 protein, human