Small breast epithelial mucin promotes the invasion and metastasis of breast cancer cells via promoting epithelial‑to‑mesenchymal transition

Oncol Rep. 2020 Aug;44(2):509-518. doi: 10.3892/or.2020.7640. Epub 2020 Jun 9.

Abstract

The aim of the present study was to observe the influence of the small breast epithelial mucin (MUCL1) (also known as SBEM) gene on migration and invasion ability of breast cancer cells and to explore the potentially involved mechanism. SBEM‑interference plasmid and SBEM‑overexpressing plasmid were constructed. SBEM‑knockdown or SBEM‑​overexpressing MCF‑7 and MDA‑MB‑231 breast cancer cells were established by lentivirus‑mediated stable transfection method. The scratch wound‑healing assay and Transwell chamber experiment were used to detect the influence of the SBEM gene on the migration and invasion abilities of MCF‑7 and MDA‑MB‑231 cells. Real‑time PCR (polymerase chain reaction) and western blotting were used to detect the expression of epithelial‑to‑mesenchymal transition (EMT)‑related markers and regulators. The cell morphology was observed after transfection. The SBEM‑knockdown or SBEM‑overexpressing MCF‑7 and MDA‑MB‑231 cells were established successfully. The migration and invasion abilities were decreased after SBEM was downregulated, and were increased after SBEM was overexpressed both in MCF‑7 and MDA‑MB‑231 cell lines. The mRNA and protein expressions of N‑cadherin, Twist and vimentin were elevated following SBEM overexpression, while the expression of E‑cadherin and claudin‑1 were found to be decreased following SBEM overexpression. In conclusion, SBEM has the potential to promote migration and invasion ability of breast cancer cells via promoting epithelial‑to‑mesenchymal transition.

Keywords: breast cancer; mucin‑like protein 1; MCF‑7 cells; MDA‑MB‑231 cells; epithelial‑to‑mesenchymal transition.

MeSH terms

  • Breast Neoplasms / pathology*
  • Cell Line, Tumor
  • Cell Movement
  • Epithelial-Mesenchymal Transition
  • Female
  • Gene Knockdown Techniques
  • Humans
  • Mucins / genetics
  • Mucins / metabolism*
  • Neoplasm Invasiveness / pathology
  • Signal Transduction

Substances

  • MUCL1 protein, human
  • Mucins