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Study · In vitro (cells) · 2005

7 results

Kisspeptin-10-induced signaling of GPR54 negatively regulates chemotactic responses mediated by CXCR4: a potential mechanism for the metastasis suppressor activity of kisspeptins.

Navenot JM, Wang Z, Chopin M, Fujii N, Peiper SC

Cancer research1 Nov 2005Cited by 66 (Europe PMC)

PMID16288036 (opens in a new tab)DOI10.1158/0008-5472.can-05-1757 (opens in a new tab)PepBankPUB-16288036
Publisher pagePubMedAsk about this study
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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 study7

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

  1. 01LabIn vitro (cells)Mechanism

    In tumor cells expressing CXCR4, kisspeptin‑10 blocked chemotaxis toward low and high concentrations of SDF-1/CXCL12.

    In plain wordsIn cells, kisspeptin‑10 stopped tumor cells from moving toward the signal SDF-1.

    Peptide
    Kisspeptin-10
    Outcome
    DecreaseSDF-1-induced chemotaxis
    Study

    n: not reported in source

    tumor cells expressing CXCR4
    Outcome group
    Cancer cell invasion and metastasis · Cancer
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Kp-10 blocked chemotaxis of tumor cells expressing CXCR4 in response to low and high concentrations of SDF-1/CXCL12 and inhibited mobilization of calcium ions induced by this ligand.
    1 context sentence
    Summary · context
    To study the mechanism by which Kp-10 antagonizes metastatic spread, the effect on CXCR4-mediated signaling, which has been shown to direct organ-specific migration of tumor cells, was determined.
  2. 02LabIn vitro (cells)Mechanism

    In tumor cells expressing CXCR4, kisspeptin‑10 inhibited calcium mobilization induced by SDF-1/CXCL12.

    In plain wordsIn cells, kisspeptin‑10 reduced the calcium signal triggered by SDF-1.

    Peptide
    Kisspeptin-10
    Outcome
    DecreaseSDF-1-induced calcium mobilization
    Study

    n: not reported in source

    tumor cells expressing CXCR4
    Outcome group
    Receptor activity and mechanism · Cancer
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Kp-10 blocked chemotaxis of tumor cells expressing CXCR4 in response to low and high concentrations of SDF-1/CXCL12 and inhibited mobilization of calcium ions induced by this ligand.
    1 context sentence
    Summary · context
    To study the mechanism by which Kp-10 antagonizes metastatic spread, the effect on CXCR4-mediated signaling, which has been shown to direct organ-specific migration of tumor cells, was determined.
  3. 03LabIn vitro (cells)Mechanism

    In tumor cells, pretreatment with kisspeptin‑10 did not down-modulate cell surface CXCR4 expression.

    In plain wordsIn cells, kisspeptin‑10 did not reduce the amount of CXCR4 on the cell surface.

    Peptide
    Kisspeptin-10
    Outcome
    No significant changeCell surface CXCR4 expression
    Study

    n: not reported in source

    tumor cells expressing CXCR4
    Outcome group
    Receptor activity and mechanism · Cancer
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Pretreatment with Kp-10 did not induce down-modulation of cell surface CXCR4 expression, reduce affinity for SDF-1/CXCL12, or alter Galphai subunit activation stimulated by this ligand.
    1 context sentence
    Summary · context
    To study the mechanism by which Kp-10 antagonizes metastatic spread, the effect on CXCR4-mediated signaling, which has been shown to direct organ-specific migration of tumor cells, was determined.
  4. 04LabIn vitro (cells)Mechanism

    In tumor cells, pretreatment with kisspeptin‑10 did not reduce CXCR4 affinity for SDF-1/CXCL12.

    In plain wordsIn cells, kisspeptin‑10 did not change how tightly CXCR4 binds SDF-1.

    Peptide
    Kisspeptin-10
    Outcome
    No significant changeCXCR4 affinity for SDF-1
    Study

    n: not reported in source

    tumor cells expressing CXCR4
    Outcome group
    Receptor activity and mechanism · Cancer
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Pretreatment with Kp-10 did not induce down-modulation of cell surface CXCR4 expression, reduce affinity for SDF-1/CXCL12, or alter Galphai subunit activation stimulated by this ligand.
    1 context sentence
    Summary · context
    To study the mechanism by which Kp-10 antagonizes metastatic spread, the effect on CXCR4-mediated signaling, which has been shown to direct organ-specific migration of tumor cells, was determined.
  5. 05LabIn vitro (cells)Mechanism

    In tumor cells, pretreatment with kisspeptin‑10 did not alter Galphai subunit activation stimulated by SDF-1/CXCL12.

    In plain wordsIn cells, kisspeptin‑10 did not change the Galphai signal triggered by SDF-1.

    Peptide
    Kisspeptin-10
    Outcome
    No significant changeGalphai subunit activation by SDF-1
    Study

    n: not reported in source

    tumor cells expressing CXCR4
    Outcome group
    Receptor activity and mechanism · Cancer
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Pretreatment with Kp-10 did not induce down-modulation of cell surface CXCR4 expression, reduce affinity for SDF-1/CXCL12, or alter Galphai subunit activation stimulated by this ligand.
    1 context sentence
    Summary · context
    To study the mechanism by which Kp-10 antagonizes metastatic spread, the effect on CXCR4-mediated signaling, which has been shown to direct organ-specific migration of tumor cells, was determined.
  6. 06LabIn vitro (cells)Mechanism

    In tumor cells, kisspeptin‑10 stimulated prolonged phosphorylation of extracellular signal-regulated kinase 1/2.

    In plain wordsIn cells, kisspeptin‑10 caused a lasting rise in ERK1/2 activation.

    Peptide
    Kisspeptin-10
    Outcome
    IncreaseERK1/2 phosphorylation
    Study

    n: not reported in source

    tumor cells expressing CXCR4
    Outcome group
    Receptor activity and mechanism · Cancer
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Kp-10 stimulated prolonged phosphorylation of extracellular signal-regulated kinase 1/2
    1 context sentence
    Summary · context
    To study the mechanism by which Kp-10 antagonizes metastatic spread, the effect on CXCR4-mediated signaling, which has been shown to direct organ-specific migration of tumor cells, was determined.
  7. 07LabIn vitro (cells)Mechanism

    In tumor cells, kisspeptin‑10 inhibited the phosphorylation of Akt induced by SDF-1.

    In plain wordsIn cells, kisspeptin‑10 reduced Akt activation triggered by SDF-1.

    Peptide
    Kisspeptin-10
    Outcome
    DecreaseSDF-1-induced Akt phosphorylation
    Study

    n: not reported in source

    tumor cells expressing CXCR4
    Outcome group
    Receptor activity and mechanism · Cancer
    Studied dose
    Dose not stated

    Source sentences

    Summary
    it inhibited the phosphorylation of Akt induced by SDF-1.
    1 context sentence
    Summary · context
    To study the mechanism by which Kp-10 antagonizes metastatic spread, the effect on CXCR4-mediated signaling, which has been shown to direct organ-specific migration of tumor cells, was determined.

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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