ArticleAmerican journal of cancer research2026
MCPB-21 targets glycogenin-2 to regulate fatty acid oxidation and promote ferroptosis of breast cancer.
Article in American journal of cancer research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
This study systematically evaluated the anti-breast cancer potential and mechanisms of the cannabidiol (CBD) derivative MCPB-21. The structure of MCPB-21 was confirmed by nuclear magnetic resonance (NMR). The study analyzed differentially expressed genes associated with breast cancer using public databases and verified the binding affinity of MCPB-21 to glycogenin-2 (GYG2) through molecular docking. Additionally, the effects of MCPB-21 on apoptosis, invasion capacity, and lipid metabolism were evaluated in MDA-MB-231 and MCF-7 breast cancer cells using flow cytometry, Transwell invasion assays, cell proliferation assays, and Oil Red O staining. Western blot was employed to examine expression changes in proteins related to fatty acid β-oxidation and ferroptosis, including Acyl-CoA Oxidase 1 (ACOX1), ATP Binding Cassette Subfamily D Member 3 (ABCD3), ATP Binding Cassette Subfamily D Member 4 (ABCD4), Peroxisomal l-bifunctional enzyme (EHHADH), Carnitine palmitoyltransferase 1α (CPT1α), Glutathione Peroxidase 4 (GPX4), Solute Carrier Family 7 Member 11 (SLC7A11), and Acyl-CoA Synthetase Long Chain Family Member 4 (ACSL4). The role of fatty acid oxidation in ferroptosis was further analyzed using the ACOX1 inhibitor 10,12-Tricosadiynoic acid (500 nM). Additionally, the effects of MCPB-21 on fatty acid oxidation and ferroptosis were evaluated by interfering with GYG2 expression. Ferrostatin-1 (Fer-1) rescue experiments were conducted to verify the dependence of MCPB-21-induced cell death. Finally, the anti-tumor efficacy of various doses of MCPB-21 was compared to the control drug CBD.
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