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Study · Not a test of the peptide alone · 2015

1 result

Metformin prevents cancer metastasis by inhibiting M2-like polarization of tumor associated macrophages.

Ding L, Liang G, Yao Z, Zhang J, Liu R, Chen H, Zhou Y, Wu H, Yang B, He Q

Oncotarget1 Nov 2015Cited by 139 (Europe PMC)

PMID26497364 (opens in a new tab)PMCIDPMC4742188 (opens in a new tab)DOI10.18632/oncotarget.5541 (opens in a new tab)PepBankPUB-26497364
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Summary

Accumulated evidence suggests that M2-like polarized tumor associated macrophages (TAMs) plays an important role in cancer progression and metastasis, establishing TAMs, especially M2-like TAMs as an appealing target for therapy intervention. Here we found that metformin significantly suppressed IL-13 induced M2-like polarization of macrophages, as illustrated by reduced expression of CD206, down-regulation of M2 marker mRNAs, and inhibition of M2-like macrophages promoted migration of cancer cells and endothelial cells. Metformin triggered AMPKα1 activation in macrophage and silencing of AMPKα1 partially abrogated the inhibitory effect of metformin in IL-13 induced M2-like polarization. Administration of AICAR, another activator of AMPK, also blocked the M2-like polarization of macrophages. Metformin greatly reduced the number of metastases of Lewis lung cancer without affecting tumor growth. In tumor tissues, the percentage of M2-like macrophage was decreased and the area of pericyte-coated vessels was increased. Further, the anti-metastatic effect of metformin was abolished when the animals were treated with macrophages eliminating agent clodronate liposome. These findings suggest that metformin is able to block the M2-like polarization of macrophages partially through AMPKα1, which plays an important role in metformin inhibited metastasis of Lewis lung cancer.
CC BYText from Europe PMC. Highlighted sentences are the source of results.

Results from this study1

No result from this study comes from a test of the peptide.

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. 01LabNot a test of AICAR (acadesine) aloneIn vitro (cells)Mechanism

    In macrophages, AICAR blocked M2-like polarization.

    In plain wordsIn cells, AICAR blocked M2-like macrophage polarization.

    Peptide
    AICAR (acadesine)
    Outcome
    DecreaseM2-like macrophage polarization
    Study

    n: not reported in source

    IL-13-stimulated macrophages
    Outcome group
    Immune response · Immune and inflammation

    Source sentences

    Summary
    Administration of AICAR, another activator of AMPK, also blocked the M2-like polarization of macrophages.

    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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