Human adipose‑derived mesenchymal stem cells promote breast cancer MCF7 cell epithelial‑mesenchymal transition by cross interacting with the TGF‑β/Smad and PI3K/AKT signaling pathways.

The influence and underlying mechanisms of human adipose‑derived stem cells (Hu‑ADSCs) on breast cancer cells in the tumor microenvironment remain unclear. Understanding the association between Hu‑ADSCs and cancer cells may provide targets for breast cancer treatment and reference for the clinical application of stem cells. Therefore, a Hu‑ADSC and breast cancer MCF7 cell coculture system was established to investigate the paracrine effects of Hu‑ADSCs on MCF7 cell migration and invasion, in addition to the potential mechanism of action by reverse transcription‑quantitative polymerase chain reaction and western blotting. Hu‑ADSCs enhanced MCF7 cell migration and invasion by decreasing the expression of epithelial marker E‑cadherin, and increasing the expression of interstitial marker N‑cadherin and epithelial‑mesenchymal transition (EMT) transcription factors in vitro. The EMT effect of cocultured MCF7 cells was inhibited with the addition of anti‑transforming growth factor (TGF)‑β1 or phosphoinositide 3‑kinase (PI3K) inhibitor LY294002, accompanied by a significant decrease in phosphorylated (p)‑mothers against decapentaplegic homolog (Smad) and p‑protein kinase B (AKT) expression. The data suggested that the paracrine effect of Hu‑ADSCs in the tumor microenvironment promoted the EMT of MCF7 cells by cross interacting with the TGF‑β/Smad and PI3K/AKT pathways.