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Study · Animal study (in vivo) · 2007

5 results

Systemic treatment with the antidiabetic drug metformin selectively impairs p53-deficient tumor cell growth.

Buzzai M, Jones RG, Amaravadi RK, Lum JJ, DeBerardinis RJ, Zhao F, Viollet B, Thompson CB

Cancer research1 Jul 2007Cited by 735 (Europe PMC)

Summary

The text of this summary is not shown here, because the article license does not allow reuse. Read it at the source (opens in a new tab)

Text rights: Publisher copyright. Results still quote short attributed sentences.

Results from this study5

5 results from studies that gave the peptide. No result from this study comes from people.

  1. 01AnimalAnimal study (in vivo)Efficacy outcome

    In vivo, AICAR selectively inhibited p53-deficient tumor growth.

    In plain wordsIn animals, AICAR selectively reduced growth of tumors without p53.

    Outcome
    Decreasep53-deficient tumor growth
    Study

    n: not reported in source

    HCT116 p53-deficient tumor xenografts
    Outcome group
    Tumor growth · Cancer
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Treatment with AICAR, another AMPK activator, also showed a selective ability to inhibit p53(-/-) tumor growth in vivo.
  2. 02LabIn vitro (cells)Mechanism

    In HCT116 cells exposed to AICAR, p53-positive cells activated autophagy, but p53-deficient cells did not.

    In plain wordsIn cells given AICAR, cells with p53 activated autophagy, but cells without p53 did not.

    Outcome
    MixedAutophagy in HCT116 cells
    Study

    n: not reported in source

    HCT116 p53-positive and p53-deficient colon cancer cells
    Outcome group
    Receptor activity and mechanism · Cancer
    Studied dose
    Dose not stated

    Source sentences

    Summary
    In the presence of either of the two drugs, HCT116 p53(+/+) cells, but not HCT116 p53(-/-) cells, activated autophagy.
    1 context sentence
    Summary · context
    Treatment with AICAR, another AMPK activator, also showed a selective ability to inhibit p53(-/-) tumor growth in vivo.
  3. 03LabIn vitro (cells)Mechanism

    In nontransformed mouse embryo fibroblasts, AICAR induced autophagy in a p53-dependent manner.

    In plain wordsIn cells from mouse embryos, AICAR-induced autophagy depended on p53.

    Outcome
    MixedAutophagy in fibroblasts
    Study

    mousen: not reported in source

    Nontransformed mouse embryo fibroblasts
    Outcome group
    Receptor activity and mechanism · Cancer
    Studied dose
    Dose not stated

    Source sentences

    Summary
    A similar p53-dependent induction of autophagy was observed when nontransformed mouse embryo fibroblasts were treated.
    1 context sentence
    Summary · context
    In the presence of either of the two drugs, HCT116 p53(+/+) cells, but not HCT116 p53(-/-) cells, activated autophagy.
  4. 04LabIn vitro (cells)Mechanism

    In mouse embryo fibroblasts, AICAR enhanced fatty acid beta-oxidation in p53-positive cells, but not p53-deficient cells.

    In plain wordsIn mouse cells, AICAR increased fatty acid burning in cells with p53, but not cells without p53.

    Outcome
    MixedFatty acid beta-oxidation
    Study

    mousen: not reported in source

    Mouse embryo fibroblasts
    Outcome group
    Mitochondrial function · Metabolic and weight
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Treatment with either metformin or AICAR also led to enhanced fatty acid beta-oxidation in p53(+/+) MEFs, but not in p53(-/-) MEFs.
  5. 05LabIn vitro (cells)Mechanism

    In p53-positive mouse embryo fibroblasts, AICAR induced more fatty acid beta-oxidation than metformin.

    In plain wordsIn mouse cells with p53, AICAR increased fatty acid burning more than metformin.

    Outcome
    IncreaseFatty acid beta-oxidation versus metformin
    Study

    mousen: not reported in source

    p53(+/+) mouse embryo fibroblasts
    Comparator
    Metformin
    Outcome group
    Mitochondrial function · Metabolic and weight
    Studied dose
    Dose not stated

    Source sentences

    Summary
    However, the magnitude of induction was significantly lower in metformin-treated cells, as metformin treatment also suppressed mitochondrial electron transport.
    1 context sentence
    Summary · context
    Treatment with either metformin or AICAR also led to enhanced fatty acid beta-oxidation in p53(+/+) MEFs, but not in p53(-/-) MEFs.

AI wrote and checked these results. AI can make mistakes, so check important results against the source.

Version history

PepBank keeps every version of the data on this study. Status changes from Retraction Watch, Europe PMC and Crossref are listed with their source.

  1. Version 2Current

    21 Oct 2026, 15:58 UTC

    Study results updated

  2. Version 1

    21 Oct 2026, 12:50 UTC

    First added · source update from Europe PMC

Subjects

Terms as the source lists them.

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