Elucidating the Anticancer Mechanism of Arachidin‐1 in Triple‐Negative Breast Cancer Cells

Abstract

Triple‐negative breast cancer (TNBC) is one of the deadliest forms of breast cancer that affects women worldwide. TNBC is unresponsive to standard hormonal cancer treatments, leading to high mortality rates. Treatment resistance and low survival rates necessitate investigating alternative treatment options for this type of cancer. Plant natural products, such as the prenylated stilbenoid arachidin‐1 from peanut, have shown cytotoxicity to certain cancer cells. To this end, the goal of this study was to examine the apoptotic effects of arachidin‐1 in TNBC cell lines MDA‐MB‐231 and MDA‐MB‐436. To produce arachidin‐1, peanut hairy root cultures were co‐treated with elicitors, and arachidin‐1 was purified from extracts of the culture medium by semi‐preparative high performance liquid chromatography. The apoptotic effects of arachidin‐1 were studied via western blotting by checking the protein levels of PARP, caspase‐8, caspase‐9, and survivin. Vinculin and GAPDH were used as protein loading controls. Results showed that as arachidin‐1 concentration increased, the amount of cleaved PARP also increased. Similarly, the levels of cleaved caspase‐9 increased as concentrations of arachidin‐1 increased. Whereas the level of survivin, an apoptosis inhibitor protein, decreased at increasing concentrations of arachidin‐1. The increased expression of cleaved PARP, cleaved caspase‐9, and reduced surviving expression in TNBC cells treated with arachidin‐1 represents the activation of intrinsic apoptosis in the cells. This accentuates the importance of expanding our understanding of the connection between stilbenoids and triple‐negative breast cancer cells. In future research, we will study the effect of arachidin‐1 on signaling pathways in TNBC cell lines.