Anticancer potential of Marsdenia tenacissima extract: modulation of proliferation, apoptosis and SBEM gene expression in triple-negative breast cancer MDA-MB-231 cells

Abstract

Marsdenia tenacissima (MT) is a herbal remedy that has been used for many years to treat cancer. While the anti-cancer properties of Marsdenia tenacissima extract (MTE) have been observed in several malignancies, its effect on the fundamental mechanisms of triple-negative breast cancer cells remains unclear. Here, we investigate the underlying anti-cancer mechanisms of MTE in MDA-MB-231 cells in regard to their proliferation, apoptosis, and the expression of the secretory breast epithelial mucin (SBEM) gene. Cell Counting Kit-8 (CCK-8) and Annexin V and propridium iodide (PI) staining kits were used to measure the proliferation and apoptosis in MDA-MB-231 cells, respectively. The effects of MTE on MDA-MB-231 cell migration were evaluated via scratch healing at 0 and 24 hours after treatment with different MTE concentrations. Western blot was used to detect the protein expressions of SBEM and apoptosis-related factors. Real-time quantitative Polymerase Chain Reaction (RT-qPCR) was performed to detect SBEM mRNA expression after different drug concentrations. CCK-8 assays indicated increased proliferation and inhibition of MDA-MB-231 cells with increasing MTE concentrations. Flow cytometry also showed a gradual dose-dependent increase in MDA-MB-231 cell apoptosis rate with increasing MTE concentrations. Additionally, MTE reduced the migration of MDA-MB-231 cells in a dose-dependent way. Proteomic experiments showed that the drug group downregulated the expression levels of B-cell Lymphoma-2 (BCL-2), B-cell lymphoma-extra large (BCL-XL) and SBEM in MDA-MB-231 cells, and RT-qPCR analysis showed that the expression of SBEM mRNA in MDA-MB-231 cells could be down-regulated in a dose-dependent manner by MTE. MTE exerted its anti-cancer effects on MDA-MB-231 cells by inhibiting their proliferation and migration, as well as inducing cell apoptosis. These effects might be associated with the down-regulation of BCL-2 and BCL-XL expression and the deregulation of SBEM mRNA expression.