Blocking Fatty Acid Storage May Induce Glioblastoma Apoptosis
Turning off an enzyme that glioblastoma cells use to store the fatty acids they feed on as energy for rapid cell division may offer a new treatment option for the deadly cancer, researchers reported (https://doi.org/10.1016/j.cmet.2020.06.002) in Cell Metabolism.
Glioblastoma cells use an enzyme called DGAT1 to convert fatty acids into triglycerides that they can safely store in their cytoplasm. Using mouse models, researchers inhibited the production of DGAT1, which caused the cancer cells to divert the fatty acids to the mitochondria. There, it overwhelmed the organelles and caused them to produce oxygen radicals, damaging the cancer cells’ mitochondria and resulting in apoptosis.
“Together, our study demonstrates that DGAT1 upregulation protects glioblastoma from oxidative damage and maintains lipid homeostasis by facilitating storage of excess fatty acids,” the researchers wrote (https://doi.org/10.1016/j.cmet.2020.06.002). “Targeting DGAT1 could be a promising therapeutic approach for glioblastoma.”
In a press release, the study’s principal investigator added (https://cancer.osu.edu/news/blocking-fat-storage-might-offer-new-way-to-treat-most-lethal-form-of-brain-cancer) that the treatment approach may also apply to prostate, colon, renal, and other cancers that use lipid formation for tumor growth.