β-elemene induced apoptosis and senescence of triple-negative breast cancer cells through IGF1/IGF1R pathway.

PURPOSE

β-elemene has a wide range of anticancer effects and can be used in a variety of cancer types. This study mainly explored its mechanism of action on TNBC cells and provided theoretical basis for the treatment of TNBC.

METHODS

Firstly, TNBC cells were treated with different concentrations of β-elemene, and screened out an appropriate concentration for subsequent research. Then, through the bioinformatics website, predicted genes that have a binding relationship with β-elemene. Then, the overexpression vector of the selected gene was transfected into the cell. The effects of β-elemene and its target genes on the proliferation and apoptosis of TNBC cells were detected by CCK-8, Edu assay, and flow cytometry, and the senescence of cells was determined by SA-β-gal experiment. Western blotting was used to detect the expression of apoptosis and aging-related proteins.

RESULTS

β-elemene inhibited TNBC cell viability and proliferation in a concentration-dependent manner, and induces apoptosis and senescence. Through the screening of candidate genes, IGF1 was finally determined to be an effective target gene of β-elemene. The expression level of IGF1 was decreased in cells treated with β-elemene. Overexpression of IGF1 significantly alleviated ability of β-elemene to inhibit cell viability, proliferation, and induced cell apoptosis and senescence. In addition, β-elemene inhibited the expression of IGF1R and Bcl-2, and promoted the expression of Cleaved Caspase-3 and senescence-related proteins (p27, p16, p53 and p21), and these effects were reversed by overexpression of IGF1.

CONCLUSION

β-elemene induced apoptosis and senescence of triple-negative breast cancer cells through IGF1/IGF1R pathway.