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Study · Animal study (in vivo) · mouse · 2016

4 results

Aerobic Exercise and Pharmacological Treatments Counteract Cachexia by Modulating Autophagy in Colon Cancer.

Pigna E, Berardi E, Aulino P, Rizzuto E, Zampieri S, Carraro U, Kern H, Merigliano S, Gruppo M, Mericskay M, Li Z, Rocchi M and 6 more

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Barone R, Macaluso F, Di Felice V, Adamo S, Coletti D, Moresi V

Scientific reports31 May 2016Cited by 155 (Europe PMC)

PMID27244599 (opens in a new tab)PMCIDPMC4886631 (opens in a new tab)DOI10.1038/srep26991 (opens in a new tab)PepBankPUB-27244599
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Summary

Recent studies have correlated physical activity with a better prognosis in cachectic patients, although the underlying mechanisms are not yet understood. In order to identify the pathways involved in the physical activity-mediated rescue of skeletal muscle mass and function, we investigated the effects of voluntary exercise on cachexia in colon carcinoma (C26)-bearing mice. Voluntary exercise prevented loss of muscle mass and function, ultimately increasing survival of C26-bearing mice. We found that the autophagic flux is overloaded in skeletal muscle of both colon carcinoma murine models and patients, but not in running C26-bearing mice, thus suggesting that exercise may release the autophagic flux and ultimately rescue muscle homeostasis. Treatment of C26-bearing mice with either AICAR or rapamycin, two drugs that trigger the autophagic flux, also rescued muscle mass and prevented atrogene induction. Similar effects were reproduced on myotubes in vitro, which displayed atrophy following exposure to C26-conditioned medium, a phenomenon that was rescued by AICAR or rapamycin treatment and relies on autophagosome-lysosome fusion (inhibited by chloroquine). Since AICAR, rapamycin and exercise equally affect the autophagic system and counteract cachexia, we believe autophagy-triggering drugs may be exploited to treat cachexia in conditions in which exercise cannot be prescribed.
CC BYText from Europe PMC. Highlighted sentences are the source of results.

Results from this study4

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

  1. 01AnimalAnimal study (in vivo)Efficacy outcome

    In C26-bearing mice, AICAR rescued muscle mass.

    In plain wordsIn mice with colon tumors, AICAR preserved muscle mass.

    Peptide
    AICAR (acadesine)
    Outcome
    IncreaseMuscle mass
    Study

    mousen: not reported in source

    C26 colon carcinoma-bearing mice
    Outcome group
    Muscle injury and repair · Musculoskeletal
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Treatment of C26-bearing mice with either AICAR or rapamycin, two drugs that trigger the autophagic flux, also rescued muscle mass and prevented atrogene induction.
  2. 02AnimalAnimal study (in vivo)Mechanism

    In C26-bearing mice, AICAR prevented atrogene induction.

    In plain wordsIn mice with colon tumors, AICAR prevented induction of muscle atrophy genes.

    Peptide
    AICAR (acadesine)
    Outcome
    DecreaseAtrogene induction
    Study

    mousen: not reported in source

    C26 colon carcinoma-bearing mice
    Outcome group
    Muscle injury and repair · Musculoskeletal
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Treatment of C26-bearing mice with either AICAR or rapamycin, two drugs that trigger the autophagic flux, also rescued muscle mass and prevented atrogene induction.
  3. 03LabIn vitro (cells)Efficacy outcome

    In myotubes exposed to C26-conditioned medium, AICAR rescued atrophy.

    In plain wordsIn cells exposed to medium from colon cancer cells, AICAR reduced muscle-cell atrophy.

    Peptide
    AICAR (acadesine)
    Outcome
    DecreaseMyotube atrophy
    Study

    n: not reported in source

    myotubes exposed to C26-conditioned medium
    Outcome group
    Muscle injury and repair · Musculoskeletal
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Similar effects were reproduced on myotubes in vitro, which displayed atrophy following exposure to C26-conditioned medium, a phenomenon that was rescued by AICAR or rapamycin treatment and relies on autophagosome-lysosome fusion (inhibited by chloroquine).

Studies that did not test the peptide alone1

In this study, AICAR (acadesine) was a lab tool or a carrier, part of a mix, or the subject of a lab method. These results are not evidence about taking AICAR (acadesine).

  1. 04LabNot a test of AICAR (acadesine) aloneIn vitro (cells)Mechanism

    In myotubes, rescue of C26-conditioned medium-induced atrophy by AICAR depended on autophagosome-lysosome fusion, inhibited by chloroquine.

    In plain wordsIn cells, AICAR protection against muscle-cell atrophy depended on autophagosome-lysosome fusion, which chloroquine inhibited.

    Peptide
    AICAR (acadesine)
    Outcome
    Not applicableAutophagosome-lysosome fusion dependence
    Study

    n: not reported in source

    myotubes exposed to C26-conditioned medium
    Outcome group
    Receptor activity and mechanism · Musculoskeletal

    Source sentences

    Summary
    Similar effects were reproduced on myotubes in vitro, which displayed atrophy following exposure to C26-conditioned medium, a phenomenon that was rescued by AICAR or rapamycin treatment and relies on autophagosome-lysosome fusion (inhibited by chloroquine).

    In this study, AICAR (acadesine) was a lab tool or a carrier, part of a mix, or the subject of a lab method. This result is not evidence about taking AICAR (acadesine).

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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