The pro-proliferative effect of insulin in human breast epithelial DMBA-transformed and non-transformed cell lines is PI3K-, mTOR- and GLUT1-dependent

Cell Biochem Funct. 2022 Mar;40(2):127-137. doi: 10.1002/cbf.3681. Epub 2022 Jan 10.

Abstract

Type 2 diabetes mellitus (T2DM) is linked to an increased risk of breast cancer. We aimed to investigate how T2DM-associated characteristics (high levels of glucose, insulin, leptin, inflammatory mediators and oxidative stress) influence breast cancer carcinogenesis, in DMBA-treated (MCF-12ADMBA ) and non-treated breast epithelial (MCF-12A) cell lines. Insulin (50 nM) promotes cell proliferation, 3 H-DG uptake and lactic acid production in both cell lines. The stimulatory effects of insulin upon cell proliferation and 3 H-DG uptake were hampered by rapamycin, LY294001 and BAY-876, in both cell lines. In conclusion, hyperinsulinemia, one important characteristic of T2DM, contributes to the initiation of breast cancer by a PI3K- and mTOR-dependent mechanism involving increased GLUT1-mediated glucose uptake. SIGNIFICANCE: The pro-proliferative effect of insulin in human breast epithelial DMBA-transformed and non-transformed cell lines is PI3K-, mTOR- and GLUT1-dependent.

Keywords: DMBA; GLUT1; PI3K; breast cancer; insulin; mTOR.

MeSH terms

  • Breast Neoplasms* / chemically induced
  • Breast Neoplasms* / metabolism
  • Cell Line, Tumor
  • Diabetes Mellitus, Type 2*
  • Female
  • Glucose Transporter Type 1 / metabolism
  • Humans
  • Insulin / metabolism
  • Insulin / pharmacology
  • Phosphatidylinositol 3-Kinases / metabolism
  • Proto-Oncogene Proteins c-akt / metabolism
  • Signal Transduction
  • TOR Serine-Threonine Kinases / metabolism

Substances

  • Glucose Transporter Type 1
  • Insulin
  • Proto-Oncogene Proteins c-akt
  • TOR Serine-Threonine Kinases