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Study · In vitro (cells) · 2011

7 results

GPR54 (KISS1R) transactivates EGFR to promote breast cancer cell invasiveness.

Zajac M, Law J, Cvetkovic DD, Pampillo M, McColl L, Pape C, Di Guglielmo GM, Postovit LM, Babwah AV, Bhattacharya M

PloS one28 Jun 2011Cited by 72 (Europe PMC)

PMID21738726 (opens in a new tab)PMCIDPMC3125256 (opens in a new tab)DOI10.1371/journal.pone.0021599 (opens in a new tab)PepBankPUB-21738726
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Summary

Kisspeptins (Kp), peptide products of the Kisspeptin-1 (KISS1) gene are endogenous ligands for a G protein-coupled receptor 54 (GPR54). Previous findings have shown that KISS1 acts as a metastasis suppressor in numerous cancers in humans. However, recent studies have demonstrated that an increase in KISS1 and GPR54 expression in human breast tumors correlates with higher tumor grade and metastatic potential. At present, whether or not Kp signaling promotes breast cancer cell invasiveness, required for metastasis and the underlying mechanisms, is unknown. We have found that kisspeptin-10 (Kp-10), the most potent Kp, stimulates the invasion of human breast cancer MDA-MB-231 and Hs578T cells using Matrigel-coated Transwell chamber assays and induces the formation of invasive stellate structures in three-dimensional invasion assays. Furthermore, Kp-10 stimulated an increase in matrix metalloprotease (MMP)-9 activity. We also found that Kp-10 induced the transactivation of epidermal growth factor receptor (EGFR). Knockdown of the GPCR scaffolding protein, β-arrestin 2, inhibited Kp-10-induced EGFR transactivation as well as Kp-10 induced invasion of breast cancer cells via modulation of MMP-9 secretion and activity. Finally, we found that the two receptors associate with each other under basal conditions, and FRET analysis revealed that GPR54 interacts directly with EGFR. The stability of the receptor complex formation was increased upon treatment of cells by Kp-10. Taken together, our findings suggest a novel mechanism by which Kp signaling via GPR54 stimulates breast cancer cell invasiveness.
CC BYText from Europe PMC. Highlighted sentences are the source of results.

Results from this study7

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

  1. 01LabIn vitro (cells)Efficacy outcome

    In human breast cancer MDA-MB-231 and Hs578T cells, kisspeptin‑10 stimulated invasion in Matrigel-coated Transwell chamber assays.

    In plain wordsIn breast cancer cells in the lab, kisspeptin‑10 made the cells invade more.

    Peptide
    Kisspeptin-10
    Outcome
    IncreaseInvasion of MDA-MB-231 and Hs578T cells (Matrigel Transwell assay)
    Study

    humann: not reported in source

    Human breast cancer cells (MDA-MB-231, Hs578T)
    Outcome group
    Tumor growth · Cancer
    Studied dose
    Dose not stated

    Source sentences

    Summary
    stimulates the invasion of human breast cancer MDA-MB-231 and Hs578T cells using Matrigel-coated Transwell chamber assays
    1 context sentence
    Summary · context
    We have found that kisspeptin-10 (Kp-10), the most potent Kp, stimulates the invasion of human breast cancer MDA-MB-231 and Hs578T cells using Matrigel-coated Transwell chamber assays and induces the formation of invasive stellate structures in three-dimensional invasion assays.
  2. 02LabIn vitro (cells)Efficacy outcome

    In human breast cancer cells, kisspeptin‑10 induced the formation of invasive stellate structures in three-dimensional invasion assays.

    In plain wordsIn breast cancer cells in the lab, kisspeptin‑10 made the cells form invasive star-shaped structures.

    Peptide
    Kisspeptin-10
    Outcome
    IncreaseInvasive stellate structures in three-dimensional invasion assays
    Study

    humann: not reported in source

    Human breast cancer cells (MDA-MB-231, Hs578T)
    Outcome group
    Tumor growth · Cancer
    Studied dose
    Dose not stated

    Source sentences

    Summary
    induces the formation of invasive stellate structures in three-dimensional invasion assays.
    1 context sentence
    Summary · context
    We have found that kisspeptin-10 (Kp-10), the most potent Kp, stimulates the invasion of human breast cancer MDA-MB-231 and Hs578T cells using Matrigel-coated Transwell chamber assays and induces the formation of invasive stellate structures in three-dimensional invasion assays.
  3. 03LabIn vitro (cells)Mechanism

    In human breast cancer cells, kisspeptin‑10 stimulated an increase in matrix metalloprotease-9 activity.

    In plain wordsIn breast cancer cells in the lab, kisspeptin‑10 raised the activity of the enzyme MMP-9.

    Peptide
    Kisspeptin-10
    Outcome
    IncreaseMatrix metalloprotease-9 activity
    Study

    humann: not reported in source

    Human breast cancer cells (MDA-MB-231, Hs578T)
    Outcome group
    Tumor growth · Cancer
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Furthermore, Kp-10 stimulated an increase in matrix metalloprotease (MMP)-9 activity.
    1 context sentence
    Summary · context
    We have found that kisspeptin-10 (Kp-10), the most potent Kp, stimulates the invasion of human breast cancer MDA-MB-231 and Hs578T cells using Matrigel-coated Transwell chamber assays and induces the formation of invasive stellate structures in three-dimensional invasion assays.
  4. 04LabIn vitro (cells)Mechanism

    In human breast cancer cells, kisspeptin‑10 induced transactivation of epidermal growth factor receptor (EGFR).

    In plain wordsIn breast cancer cells in the lab, kisspeptin‑10 switched on the EGFR growth receptor.

    Peptide
    Kisspeptin-10
    Outcome
    IncreaseEGFR transactivation
    Study

    humann: not reported in source

    Human breast cancer cells (MDA-MB-231, Hs578T)
    Outcome group
    Tumor growth · Cancer
    Studied dose
    Dose not stated

    Source sentences

    Summary
    We also found that Kp-10 induced the transactivation of epidermal growth factor receptor (EGFR).
    1 context sentence
    Summary · context
    We have found that kisspeptin-10 (Kp-10), the most potent Kp, stimulates the invasion of human breast cancer MDA-MB-231 and Hs578T cells using Matrigel-coated Transwell chamber assays and induces the formation of invasive stellate structures in three-dimensional invasion assays.
  5. 05LabIn vitro (cells)Mechanism

    In human breast cancer cells, kisspeptin‑10 treatment increased the stability of the GPR54-EGFR receptor complex.

    In plain wordsIn breast cancer cells in the lab, kisspeptin‑10 made the link between the two receptors more stable.

    Peptide
    Kisspeptin-10
    Outcome
    IncreaseStability of GPR54-EGFR receptor complex
    Study

    humann: not reported in source

    Human breast cancer cells (MDA-MB-231, Hs578T)
    Outcome group
    Tumor growth · Cancer
    Studied dose
    Dose not stated

    Source sentences

    Summary
    The stability of the receptor complex formation was increased upon treatment of cells by Kp-10.
    1 context sentence
    Summary · context
    We have found that kisspeptin-10 (Kp-10), the most potent Kp, stimulates the invasion of human breast cancer MDA-MB-231 and Hs578T cells using Matrigel-coated Transwell chamber assays and induces the formation of invasive stellate structures in three-dimensional invasion assays.

Studies that did not test the peptide alone2

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. 06LabNot a test of Kisspeptin-10 aloneIn vitro (cells)Mechanism

    In human breast cancer cells, knockdown of beta-arrestin 2 inhibited kisspeptin‑10-induced EGFR transactivation.

    In plain wordsIn breast cancer cells in the lab, removing beta-arrestin 2 reduced the EGFR activation that kisspeptin‑10 caused.

    Peptide
    Kisspeptin-10
    Outcome
    DecreaseKp-10-induced EGFR transactivation with beta-arrestin 2 knockdown
    Study

    humann: not reported in source

    Human breast cancer cells (MDA-MB-231, Hs578T)
    Outcome group
    Tumor growth · Cancer

    Source sentences

    Summary
    Knockdown of the GPCR scaffolding protein, β-arrestin 2, inhibited Kp-10-induced EGFR transactivation as well as Kp-10 induced invasion of breast cancer cells via modulation of MMP-9 secretion and activity.
    1 context sentence
    Summary · context
    We have found that kisspeptin-10 (Kp-10), the most potent Kp, stimulates the invasion of human breast cancer MDA-MB-231 and Hs578T cells using Matrigel-coated Transwell chamber assays and induces the formation of invasive stellate structures in three-dimensional invasion assays.

    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. 07LabNot a test of Kisspeptin-10 aloneIn vitro (cells)Mechanism

    In human breast cancer cells, knockdown of beta-arrestin 2 inhibited kisspeptin‑10-induced invasion, via modulation of MMP-9 secretion and activity.

    In plain wordsIn breast cancer cells in the lab, removing beta-arrestin 2 reduced the invasion that kisspeptin‑10 caused.

    Peptide
    Kisspeptin-10
    Outcome
    DecreaseKp-10-induced invasion and MMP-9 with beta-arrestin 2 knockdown
    Study

    humann: not reported in source

    Human breast cancer cells (MDA-MB-231, Hs578T)
    Outcome group
    Tumor growth · Cancer

    Source sentences

    Summary
    Knockdown of the GPCR scaffolding protein, β-arrestin 2, inhibited Kp-10-induced EGFR transactivation as well as Kp-10 induced invasion of breast cancer cells via modulation of MMP-9 secretion and activity.
    1 context sentence
    Summary · context
    We have found that kisspeptin-10 (Kp-10), the most potent Kp, stimulates the invasion of human breast cancer MDA-MB-231 and Hs578T cells using Matrigel-coated Transwell chamber assays and induces the formation of invasive stellate structures in three-dimensional invasion assays.

    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.

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