CD155 contributes to the mesenchymal phenotype of triple-negative breast cancer

Cancer Sci. 2020 Feb;111(2):383-394. doi: 10.1111/cas.14276. Epub 2020 Jan 2.

Abstract

Patients with triple-negative breast cancer (TNBC) lack molecular targets and have an unfavorable outcome. CD155 is overexpressed in human cancers, but whether it plays a role in TNBC is unexplored. Here we found that CD155 was enriched in both TNBC cell lines and tumor tissues. High CD155 expression was related to poor prognosis of breast cancer patients. CD155 was associated with a mesenchymal phenotype. CD155 knockdown induced a mesenchymal-epithelial transition in TNBC cells, and suppressed TNBC cell migration, invasion and metastasis in vitro and in vivo. Mechanistically, CD155 cross-talked with oncogenic IL-6/Stat3 and TGF-β/Smad3 pathways. Moreover, CD155 knockdown inhibited TNBC cell growth and survival. Taken together, these data indicate that CD155 contributes to the aggressive behavior of TNBC; targeting CD155 may be beneficial to these patients.

Keywords: CD155; invasion; mesenchymal-epithelial transition; metastasis.

MeSH terms

  • Cell Line, Tumor
  • Cell Movement
  • Cell Proliferation
  • Epithelial-Mesenchymal Transition
  • Female
  • Gene Expression Regulation, Neoplastic
  • Gene Knockdown Techniques
  • Humans
  • MCF-7 Cells
  • Neoplasm Metastasis
  • Neoplasm Transplantation
  • Prognosis
  • Receptors, Virus / genetics
  • Receptors, Virus / metabolism*
  • Signal Transduction
  • Triple Negative Breast Neoplasms / genetics
  • Triple Negative Breast Neoplasms / metabolism
  • Triple Negative Breast Neoplasms / pathology*
  • Up-Regulation*

Substances

  • Receptors, Virus
  • poliovirus receptor