Skip to content

Study · Not a test of the peptide alone · 2016

3 results

KISS1R signaling promotes invadopodia formation in human breast cancer cell via β-arrestin2/ERK.

Goertzen CG, Dragan M, Turley E, Babwah AV, Bhattacharya M

Cellular signalling23 Dec 2015Cited by 47 (Europe PMC)

PMID26721186 (opens in a new tab)DOI10.1016/j.cellsig.2015.12.010 (opens in a new tab)PepBankPUB-26721186
Publisher pagePubMedAsk about this study
Jump to 3 results

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 study3

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

Studies that did not test the peptide alone3

In this study, Kisspeptin-10 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 Kisspeptin-10.

  1. 01LabNot a test of Kisspeptin-10 aloneIn vitro (cells)Mechanism

    In triple negative breast cancer cells, depletion of the kisspeptin receptor KISS1R reduced the mesenchymal phenotype and invasiveness.

    In plain wordsIn human breast cancer cells in a lab dish, removing the kisspeptin receptor made the cells less invasive.

    Peptide
    Kisspeptin-10
    Outcome
    DecreaseMesenchymal phenotype and invasiveness after KISS1R depletion
    Study

    humann: not reported in source

    Triple negative breast cancer cells
    Outcome group
    Cancer cell invasion and metastasis · Cancer

    Source sentences

    Summary
    We found that depletion of KISS1R reduced their mesenchymal phenotype and invasiveness.
    1 context sentence
    Summary · context
    To further define the mechanisms by which KISS1R stimulates invasion, we determined the effect of down-regulating KISS1R expression in triple negative breast cancer cells.

    In this study, Kisspeptin-10 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 Kisspeptin-10.

  2. 02LabNot a test of Kisspeptin-10 aloneIn vitro (cells)Mechanism

    In triple negative breast cancer cells, KISS1R signaling induced invadopodia formation and activation of cortactin, cofilin and MT1-MMP.

    In plain wordsIn human breast cancer cells in a lab dish, kisspeptin receptor signaling drove formation of invasion structures called invadopodia.

    Peptide
    Kisspeptin-10
    Outcome
    IncreaseInvadopodia formation by KISS1R signaling
    Study

    humann: not reported in source

    Triple negative breast cancer cells
    Outcome group
    Cancer cell invasion and metastasis · Cancer

    Source sentences

    Summary
    We show for the first time that KISS1R signaling induces invadopodia formation and activation of key invadopodia proteins, cortactin, cofilin and membrane type I matrix metalloproteases (MT1-MMP).
    1 context sentence
    Summary · context
    To further define the mechanisms by which KISS1R stimulates invasion, we determined the effect of down-regulating KISS1R expression in triple negative breast cancer cells.

    In this study, Kisspeptin-10 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 Kisspeptin-10.

  3. 03LabNot a test of Kisspeptin-10 aloneIn vitro (cells)Mechanism

    In triple negative breast cancer cells, KISS1R-stimulated invadopodia formation occurred through a beta-arrestin2 and ERK1/2-dependent pathway, independent of Src.

    In plain wordsIn human breast cancer cells in a lab dish, the receptor drove invasion structures through a beta-arrestin2 and ERK1/2 pathway.

    Peptide
    Kisspeptin-10
    Outcome
    Not applicablePathway of KISS1R-stimulated invadopodia formation
    Study

    humann: not reported in source

    Triple negative breast cancer cells
    Outcome group
    Receptor activity and mechanism · Cancer

    Source sentences

    Summary
    Moreover, KISS1R stimulated invadopodia formation occurs via a new pathway involving a β-arrestin2 and ERK1/2-dependent mechanism, independent of Src.
    1 context sentence
    Summary · context
    To further define the mechanisms by which KISS1R stimulates invasion, we determined the effect of down-regulating KISS1R expression in triple negative breast cancer cells.

    In this study, Kisspeptin-10 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 Kisspeptin-10.

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

    10 Oct 2026, 09:43 UTC

    Study results updated

  2. Version 1

    9 Oct 2026, 03:04 UTC

    First added · source update from Europe PMC

Subjects

Terms as the source lists them.

PepBank is a research reference. Talk to a doctor before you use any peptide.