7-Ketositosterol

7-Ketositosterol is an orally active inducer of apoptosis and ferroptosis. 7-Ketositosterol inhibits the phosphorylation of ERK1/2 and NF-κB, promotes the opening of the mitochondrial/apoptotic pathway, and induces ferroptosis in macrophages by increasing the levels of malondialdehyde, Fe²⁺ and ROS. 7-Ketositosterol upregulates the expression of gut microbiota-dependent PDLIM3, activates the p38MAPK/NF-κB signaling pathway, alters the composition of gut microbiota, increases the abundance of pathogenic bacteria, and exacerbates colitis in mice. 7-Ketositosterol can be used in studies related to breast cancer, liver cancer, and colitis^[1][2][3]. In Vitro:7-Ketositosterol (30 µM; 24 h) reduces viability of human breast MCF-7 and liver HepG2 cancer cells by ~30% and ~25%, respectively, but does not affect viability of non-cancerous BJ fibroblasts^[1].
7-Ketositosterol (30 µM; 24 h) significantly suppresses phosphorylation of ERK1/2 and NF-κB p65 (Ser536) in human breast MCF-7 and liver HepG2 cancer cells^[1].
7-Ketositosterol (30 µM; 24 h) significantly suppresses PCNA protein levels in human breast MCF-7 and liver HepG2 cancer cells, indicating reduced cell proliferation^[1].
7-Ketositosterol (30 µM; 24 h) significantly increases intracellular C₁₈-C₂₄ ceramide levels and reduces S1P levels in human breast MCF-7 and liver HepG2 cancer cells^[1].
7-Ketositosterol (30 µM; 24 h) significantly induces apoptosis in human breast MCF-7 and liver HepG2 cancer cells, as measured by TUNEL staining and annexin V-FITC/PI flow cytometry^[1].
7-Ketositosterol (1 µM; 24 h) induces M1 polarization and ferroptosis in RAW 264.7 macrophages by disrupting the ALKBH5-GCLM axis, reducing glutathione biosynthesis, and increasing oxidative stress and iron accumulation^[2].
7-Ketositosterol does not directly stimulate the growth of Staphylococcus lentus in cell-free bacterial cultures^[3]. In Vivo:7-Ketositosterol (20-100 mg/kg/day; p.o.; daily; 21 days) exacerbates DSS-induced ulcerative colitis in female C57BL/6 mice in a dose-dependent manner, and drives pro-inflammatory M1 macrophage polarization^[2].