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  1. Home
  2. Anthocyanins Prevent The Development And Progression Of Urethane-induced Lung Cancer By Regulating Energy Metabolism In Mice.
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  2. Anthocyanins Prevent The Development And Progression Of Urethane-induced Lung Cancer By Regulating Energy Metabolism In Mice.

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Anthocyanins prevent the development and progression of urethane-induced lung cancer by regulating energy metabolism

Han Luo1,2, Mengyuan Gao1,2, Hong Lu1,2

  • 1Department of Nutrition and Food Hygiene, School of Public Health, Chongqing Medical University, Chongqing, P.R. China.

Food & Nutrition Research
|May 8, 2024

View abstract on PubMed

Summary
This summary is machine-generated.

Anthocyanin (ACN) shows protective effects against lung cancer development. This natural antioxidant inhibits tumor growth and alters lipid metabolism, suggesting potential therapeutic benefits.

Keywords:
anthocyaninenergy metabolismlung cancer

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Area of Science:

  • Biochemistry
  • Oncology
  • Nutraceuticals

Background:

  • Anthocyanins (ACN) are natural antioxidants with diverse biological activities.
  • Lung cancer remains a leading cause of cancer-related mortality worldwide.
  • Understanding natural compounds' effects on cancer progression is crucial for developing novel therapies.

Purpose of the Study:

  • To evaluate the protective effect of Anthocyanin (ACN) against lung cancer development and progression.
  • To elucidate the underlying mechanisms of ACN's action in lung cancer.
  • To investigate the impact of cyanidin-3-O-glucoside chloride (C3G) on lung cancer cell viability.

Main Methods:

  • In vivo studies using C57BL/6J mice fed an ACN-supplemented or control diet, followed by urethane-induced lung cancer.
  • In vitro studies using lung cancer cell lines treated with cyanidin-3-O-glucoside chloride (C3G).
  • Analysis of tumor burden, oxidative phosphorylation, fatty acid degradation pathways, cell proliferation, and apoptosis.
  • Main Results:

    • ACN-fed mice exhibited reduced lung tumor burden compared to controls.
    • Downregulation of oxidative phosphorylation and fatty acid degradation pathways was observed in ACN-fed mice.
    • C3G significantly inhibited proliferation and induced apoptosis in A549 lung cancer cells.
    • C3G modulated the AMPK/mTOR signaling pathway, affecting fatty acid metabolism and lipid accumulation.

    Conclusions:

    • Anthocyanin (ACN) demonstrates inhibitory effects on the development and progression of urethane-induced lung tumors in mice.
    • ACN alters tumor lipid metabolism, potentially through the AMPK/mTOR pathway.
    • These findings suggest ACN's potential as a chemopreventive or therapeutic agent for lung cancer.