MIIP functions as a novel ligand for ITGB3 to inhibit angiogenesis and tumorigenesis of triple-negative breast cancer

Cell Death Dis. 2022 Sep 21;13(9):810. doi: 10.1038/s41419-022-05255-0.

Abstract

Migration and invasion inhibitory protein (MIIP) has been identified as a tumor suppressor in various cancer types. Although MIIP is reported to exert tumor suppressive functions by repressing proliferation and metastasis of cancer cells, the detailed mechanism is poorly understood. In the present study, we found MIIP is a favorable indicator of prognosis in triple-negative breast cancer. MIIP could inhibit tumor angiogenesis, proliferation, and metastasis of triple-negative breast cancer cells in vivo and in vitro. Mechanistically, MIIP directly interacted with ITGB3 and suppressed its downstream signaling. As a result, β-catenin was reduced due to elevated ubiquitin-mediated degradation, leading to downregulated VEGFA production and epithelial mesenchymal transition. More importantly, we found RGD motif is essential for MIIP binding with ITGB3 and executing efficient tumor-suppressing effect. Our findings unravel a novel mechanism by which MIIP suppresses tumorigenesis in triple-negative breast cancer, and MIIP is thus a promising molecular biomarker or therapeutic target for the disease.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Carcinogenesis / genetics
  • Carrier Proteins / metabolism
  • Cell Line, Tumor
  • Cell Movement
  • Cell Proliferation
  • Cell Transformation, Neoplastic
  • Epithelial-Mesenchymal Transition / genetics
  • Humans
  • Integrin beta3 / genetics
  • Integrin beta3 / metabolism
  • Intracellular Signaling Peptides and Proteins / metabolism
  • Ligands
  • Triple Negative Breast Neoplasms* / genetics
  • Ubiquitins / metabolism
  • beta Catenin* / metabolism

Substances

  • Carrier Proteins
  • ITGB3 protein, human
  • Integrin beta3
  • Intracellular Signaling Peptides and Proteins
  • Ligands
  • MIIP protein, human
  • Ubiquitins
  • beta Catenin