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  11. Naringenin Enhances The Efficacy Of Ferroptosis Inducers By Attenuating Aerobic Glycolysis By Activating The Ampk-pgc1α Signalling Axis In Liver Cancer

Naringenin enhances the efficacy of ferroptosis inducers by attenuating aerobic glycolysis by activating the AMPK-PGC1α signalling axis in liver cancer

Yong-Zhuo Li1, Jing Deng2, Xiao-Dong Zhang3

  • 1Department of Physiology, School of Preclinical Medicine, Guangxi Medical University, Nanning, Guangxi, China.

Heliyon
|June 24, 2024

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Preparation of Naringenin Solution for In Vivo Application
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Preparation of Naringenin Solution for In Vivo Application

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Author Spotlight: Tracing the Ferroptotic Signatures and Cell Death Dynamics in Medulloblastoma for Advanced Therapeutics
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Transfer of Manipulated Tumor-associated Neutrophils into Tumor-Bearing Mice to Study their Angiogenic Potential In Vivo
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Transfer of Manipulated Tumor-associated Neutrophils into Tumor-Bearing Mice to Study their Angiogenic Potential In Vivo

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View abstract on PubMed

Summary
This summary is machine-generated.

Naringenin enhances ferroptosis inducers

Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • Liver cancer exhibits poor treatment response and outcomes.
  • Ferroptosis, a cell death pathway, is a promising therapeutic target.
  • Naringenin modulates lipid metabolism and may enhance ferroptosis.

Purpose of the Study:

  • To investigate the synergistic effects of naringenin and ferroptosis inducers in liver cancer.
  • To explore the underlying molecular mechanisms of this combination therapy.

Main Methods:

  • Utilized liver cancer cell lines and xenograft mouse models.
  • Administered naringenin in combination with ferroptosis inducers (erastin, RSL3, sorafenib).
  • Analyzed phenotypic outcomes, lipid peroxidation, and the AMPK-PGC1α signaling pathway.
Keywords:
AMPK-PGC1α signalling axisAerobic glycolysisFerroptosisLiver cancer

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Transfer of Manipulated Tumor-associated Neutrophils into Tumor-Bearing Mice to Study their Angiogenic Potential In Vivo
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Main Results:

  • Naringenin significantly enhanced the anticancer effects of ferroptosis inducers at non-toxic doses.
  • Combination therapy demonstrated synergistic effects, increasing lipid peroxidation and ferroptotic cell death.
  • Naringenin's mechanism involves inhibiting aerobic glycolysis via the AMPK-PGC1α axis, reducing ferroptosis resistance.

Conclusions:

  • Naringenin potentiates liver cancer cell sensitivity to ferroptosis inducers.
  • The AMPK-PGC1α pathway is crucial for naringenin's synergistic effect.
  • This combination therapy holds potential for clinical translation in liver cancer treatment.
Naringenin