High glucose and high insulin conditions promote MCF‑7 cell proliferation and invasion by upregulating IRS1 and activating the Ras/Raf/ERK pathway.

Diabetes mellitus is associated with an increased risk of breast cancer, but the molecular mechanism underlying this association remains unclear. The aim of the present study was to investigate the effect of high glucose and high insulin conditions on MCF‑7 breast cancer cells and to elucidate the molecular mechanisms underlying these effects. High glucose and high insulin conditions resulted in increased viability, proliferation, and invasion in MCF‑7 cells compared with normal glucose and low insulin conditions. Reverse transcription‑quantitative polymerase chain reaction and western blot analyses revealed that insulin receptor substrate 1 (IRS1) was significantly upregulated following high glucose and high insulin treatment compared with normal glucose and low insulin conditions. Furthermore, high glucose and high insulin treatment increased the Ras family of proto‑oncogenes (Ras) and RAF1 proto‑oncogene (Raf‑1) protein expression, and activated the phosphorylation of extracellular signal‑regulated kinase (ERK) 1/2. These findings suggest that high glucose and high insulin conditions promoted the proliferation and invasion of MCF‑7 cells by upregulating IRS1 and activating the Ras/Raf/ERK pathway.