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Study · Not a test of the peptide alone · 2018

5 results

PIK3CA mutation sensitizes breast cancer cells to synergistic therapy of PI3K inhibition and AMPK activation.

Liu S, Tang Y, Yan M, Jiang W

Investigational new drugs5 Mar 2018Cited by 11 (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

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

Studies that did not test the peptide alone5

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. 01AnimalNot a test of AICAR (acadesine) aloneAnimal study (in vivo)Efficacy outcome

    In xenograft models, combined PI3K inhibition and AMPK activation attenuated tumorigenesis of parental MCF-7 cells.

    In plain wordsIn animal xenografts, combined PI3K inhibition and AMPK activation reduced tumor formation from parental MCF-7 cells.

    Outcome
    DecreaseTumorigenesis in parental cells
    Study

    n: not reported in source

    MCF-7 tumor xenografts
    Outcome group
    Tumor growth · Cancer

    Source sentences

    Summary
    Furthermore, PI3Ki&AMPKa significantly attenuated tumorigenesis of parental MCF-7 cells but not PIK3CA wild-type isogenic MCF-7 cells in tumor xenograft models.

    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).

  2. 02AnimalNot a test of AICAR (acadesine) aloneAnimal study (in vivo)Efficacy outcome

    In xenograft models, combined PI3K inhibition and AMPK activation did not attenuate tumorigenesis of PIK3CA wild-type isogenic MCF-7 cells.

    In plain wordsIn animal xenografts, the combination did not reduce tumor formation from PIK3CA wild-type isogenic MCF-7 cells.

    Outcome
    No significant changeTumorigenesis in wild-type isogenic cells
    Study

    n: not reported in source

    PIK3CA wild-type isogenic MCF-7 xenografts
    Outcome group
    Tumor growth · Cancer

    Source sentences

    Summary
    Furthermore, PI3Ki&AMPKa significantly attenuated tumorigenesis of parental MCF-7 cells but not PIK3CA wild-type isogenic MCF-7 cells in tumor xenograft models.

    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).

  3. 03LabNot a test of AICAR (acadesine) aloneIn vitro (cells)Efficacy outcome

    In MCF-7, MDA-MB-361 and HCC38 cells, GDC-0941 plus AICAR synergistically suppressed growth.

    In plain wordsIn breast cancer cells, GDC-0941 plus AICAR synergistically suppressed growth.

    Outcome
    DecreaseCell growth
    Study

    n: not reported in source

    Breast cancer cells
    Outcome group
    Tumor growth · Cancer

    Source sentences

    Summary
    Here we clearly observed synergistic suppression of cell growth in all three breast cancer cell lines (MCF-7, MDA-MB-361 and HCC38) when co-treating cells with PI3K inhibitor GDC-0941 and AMPK activator AICAR (5-Aminoimidazole-4-carboxamide ribonucleotide).

    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).

  4. 04LabNot a test of AICAR (acadesine) aloneIn vitro (cells)Efficacy outcome

    In breast cancer cells, GDC-0941 plus AICAR showed stronger synergy in PIK3CA-mutant cells than wild-type cells.

    In plain wordsIn breast cancer cells, the combination showed stronger synergy in PIK3CA-mutant cells than wild-type cells.

    Outcome
    IncreaseMutation-dependent synergy
    Study

    n: not reported in source

    Breast cancer cells
    Comparator
    PIK3CA wild-type HCC38 cells
    Outcome group
    Tumor growth · Cancer

    Source sentences

    Summary
    What is more, it is rather remarkable that the synergistic effect was much more dramatic in PIK3CA (PI3K catalytic subunit alpha) mutated (E545K) cells (MCF-7 and MDA-MB-361) than in PIK3CA wild-type cells (HCC38), which implied there is a relationship between PI3K genetic status and the efficacy of…

    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).

  5. 05LabNot a test of AICAR (acadesine) aloneIn vitro (cells)Mechanism

    In MCF-7 cells, reversal of PIK3CA E545K to wild type impaired synergy between PI3K inhibition and AICAR-mediated AMPK activation.

    In plain wordsIn cells, reversal of the PIK3CA mutation reduced synergy between PI3K inhibition and AMPK activation.

    Outcome
    DecreaseSynergy after PIK3CA reverse mutation
    Study

    n: not reported in source

    Breast cancer cells
    Comparator
    Parental MCF-7 cells
    Outcome group
    Tumor growth · Cancer

    Source sentences

    Summary
    By using PIK3CA wild-type isogenic MCF-7 cell line, which exhibited attenuated cell proliferation compared with the parental MCF-7 cell line, we found endogenous reverse mutation of PIK3CA E545K alleles to wild-type sequence in MCF-7 cells dramatically impaired the synergy of PI3Ki&AMPKa (combinator…

    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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