fig1

Figure 1. Cholesterol metabolism promotes chemoresistance. The SREBPs are a family of transcription factors. The mature active form of SREBP is generated within the Golgi apparatus by the cleavage of the precursor protein. Active forms of SREBP then translocate to the nucleus, where they promote transcription of genes involved in FA synthesis and cholesterol metabolism, including HMGCR and LDLR. HMGCR stimulates the synthesis of cholesterol. LDLR facilitates the internalization of cholesterol-carrying lipoproteins into cells. This results in the accumulation of cholesterol, predominantly within lipid raft domains, which, in turn, promotes AKT signaling and resistance to chemotherapy. Created with BioRender.com. HMGCR: 3-Hydroxy-3-methylglutaryl coenzyme A reductase; LDLR: low-density lipoprotein receptor; PI3K: phosphoinositide 3-kinase; AKT: protein kinase B.