Hispolon, A Bioactive Compound fromPhellinus linteus, Induces Apoptosis of Human Breast Cancer Cells Through the Modulation of Oxidative Stress and Autophagy

Breast cancer (BC) is a major type of cancer found in women worldwide, accounting for more than 25% of all females diagnosed as BC patients. The BC treatment still needs to be highly effective with few adverse effects on the rest of the body. This study's objective was to investigate how hispolon enhanced anticancer activities and examine the underlying processes in human breast cancer cells. Hispolon was used to treat the HTB-26 cell lines. We investigated cell viability, intracellular reactive oxygen species (ROS) production, immunofluorescence straining, MDC assay, and RT-PCR. According to the findings, hispolon inhibited HTB-26 cells from proliferating and caused them to undergo apoptosis. When the mechanism of action of hispolon was investigated, it was discovered that BCL-2 expression was downregulated while pro-apoptotic genes including caspase-3, caspase-9, and BAX were upregulated. The level of intracellular ROS was also shown to be increased by hispolon, and the expression of antioxidant genes including SOD, GPX, and Catalase was found to be downregulated. The increase in the confocal fluorescence image of LC3I/II and the identification of upregulated autophagy-related genes, such as LC3I/II, ATG5, ATG10, and ATG12, served as indicators of the activation of autophagy. Therefore, our findings showed that hispolon had great potential for being an effective therapeutic agent and could cause cell death in breast cancer cells.