Alterations in lipid metabolism and blood profile in gynecological cancers – potential strategies in diagnosis and treatment

Figures

• 

  FIGURE 1. Schematic representation of the changes in the expression of various genes encoding enzymes and other proteins related to lipid metabolism, transport and regulation in gynecological cancers. Note: The schematic illustrates changes in the expression of key genes and proteins involved in fatty acid uptake, mitochondrial β-oxidation, lipid synthesis, and signaling in endometrial cancer (EC, orange), cervical cancer (CC, blue), and ovarian cancer (OC, green). CD36, FABP4, FATP1/4, and LDLR regulate lipid uptake, with CD36 and FABP4 upregulated in OC and CC but reduced in EC. CPT1 supports mitochondrial fatty acid oxidation, particularly in OC. Enzymes of de novo lipogenesis, including ACLY, ACC, FASN, and SCD1, are consistently upregulated, driving palmitate synthesis, desaturation, and membrane remodeling. ELOVL6 and DGAT1 contribute to FA elongation and lipid droplet formation. LPA and its receptors (LPAR1/3) activate PI3K/Akt and MAPK/ERK pathways, promoting tumor proliferation, invasion, and chemoresistance. Arrows indicate upregulation (↑) or downregulation (↓) of gene expression/protein activity in specific gynecological cancers. Abbreviations: ACC–acetyl-CoA carboxylase;…

• 

  FIGURE 2. Targeting enzymes and other proteins involved in lipid metabolism for gynecological cancers therapy. The schematic illustrates the main nodes of lipid metabolism that can be targeted in gynecological cancers. Potential interventions include: inhibition of FA uptake (FABP4, CD36), FA synthesis (ACC, ACLY, FASN, SCD1, ELOVL), FA storage (DGAT1, ACAT), and FA oxidation (CPT1). Cholesterol uptake (LDLR) and mevalonate pathway enzymes (HMGCR) are also shown as therapeutic targets. Red boxes indicate representative inhibitors, siRNAs, shRNAs, knockdown approaches, or small molecules currently reported to interfere with these processes in preclinical models. Together, these interventions aim to reduce lipid availability for membrane biosynthesis, signaling, and energy production, thereby impairing cancer cell survival, proliferation, migration, and resistance mechanisms.