Sanggenol L Induces Apoptotic Cell Death by Activating the Caspase/AIF/p53 Signaling Pathway in Breast Carcinoma

Background Breast carcinoma is a deadly malignancy with a greater risk of morbidity and death, which has contributed significantly to the sharp rise in cancer cases. It has a recognized impartial effect on women. The need for a variety of treatment choices is prompted by the current therapy modules’ lack of effectiveness and adverse effects. Objectives In the present investigation, we examined the therapeutic value of Sanggenol L (San L) in human breast carcinoma cells. San L impacts on carcinoma of the breast cells are not fully understood in terms of its molecular and cellular pathways. Materials and Methods In order to assess the effectiveness of San L, this investigation employs a number of qualitative approaches, such as cytotoxicity analysis, sulforhodamine B (SRB), 4′,6-diamidino-2-phenylindole (DAPI), reactive oxygen species (ROS), and cell cycle assessment, which were conducted using breast cancer BT-474 cells. Additionally, cell death caused by San L through caspase-dependent and independent apoptosis has been investigated with western blot analysis. Results and Conclusion San L therapy significantly diminished the ability of BT-474 breast carcinoma cells to proliferate and impeded colony formation while having no impact on HBL-100 normal breast epithelial cells in a dose- and time-dependent way. San L treatment resulted in cell cycle arrest and cell death in breast carcinoma cells, which were characterized by acridine orange/ethidium bromide (AO/EtBr), DAPI, and flow cytometry at time-dependent way. The present study also explained that the half-maximal inhibitory concentration (IC 50 ) concentration of (21 and 17.3 µM/mL) San L treatment induced caspase-dependent apoptosis [enhanced the expression of Bax and decreased the expression of B-cell lymphoma 2 (Bcl-2), procaspase-3, -8, and -9], stimulation of caspase-independent apoptosis [upregulation of apoptosis-inducing factor (AIF) and endonuclease G (Endo G) on cytosol], and suppression of cell cycle [downstairs regulation of cyclin-dependent kinase 1/2 (CDK1/2), cyclin D1, cyclin E, or upregulation of p53] in breast tumor cells. According to these findings, San L causes both caspase-dependent and independent apoptosis by triggering p53 in breast carcinoma cells.