SLT reduces ovarian cancer cell viability through ROS-mediated p53 activation, causing G1 cell cycle arrest, apoptosis, and inhibition of EMT. SLT’s anticancer mechanism is likely mediated by ROS accumulation, which activates the p53 pathway, leading to cell cycle arrest, apoptosis, and reduced migration/invasion. Furthermore, SLT modulates the tumor immune microenvironment by promoting M1 macrophage plarization and suppressing M2 polarization. These effects may aid in discovering new anti-ovarian cancer therapies. The gene discussed is TP53; the disease is neoplasm.