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Bioengineer
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miR-139-5p Triggers Ferroptosis to Halt Glioma
- A study in Cell Death Discovery reveals miR-139-5p's key role in triggering ferroptosis in glioma by targeting HMG-CoA reductase.
- miR-139-5p regulates ferroptosis by suppressing HMG-CoA reductase, impacting mevalonate pathway and lipid metabolism in glioma cells.
- The study highlights miR-139-5p as an endogenous activator of ferroptotic cell death, offering a potential anti-cancer strategy.
- Overexpression of miR-139-5p inhibits glioma cell proliferation and invasion while attenuating tumor growth by inducing ferroptosis.
- HMG-CoA reductase downregulation mimics statin effects, suggesting a targeted local therapeutic approach against gliomas.
- miR-139-5p downregulation of HMG-CoA reductase disrupts supply of isoprenoids, intensifying oxidative stress and promoting ferroptosis.
- The study underscores the potential of microRNA-based therapeutics and combinational regimens for glioma treatment.
- Findings emphasize miR-139-5p's broader implications in cancer biology, highlighting targeting lipid metabolism and ferroptosis in precision oncology.
- Advanced molecular biology techniques and preclinical models validate miR-139-5p's role in glioma progression and ferroptosis induction.
- The study's insights pave the way for transformative molecular therapies targeting glioma metabolism and cell fate decisions.
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