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Study · In vitro (cells) · 2005

5 results

Activation of GPR54 promotes cell cycle arrest and apoptosis of human tumor cells through a specific transcriptional program not shared by other Gq-coupled receptors.

Becker JA, Mirjolet JF, Bernard J, Burgeon E, Simons MJ, Vassart G, Parmentier M, Libert F

Biochemical and biophysical research communications1 Jan 2005Cited by 45 (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

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

  1. 01LabIn vitro (cells)Mechanism

    In MDA-MB-435S cells expressing GPR54, kisspeptin‑10 produced a distinct pattern of gene regulation compared with the bradykinin B2 receptor, despite common Gq/11 coupling.

    In plain wordsIn cells, kisspeptin‑10 changed gene activity in a different pattern from the bradykinin B2 receptor.

    Outcome
    Not applicableGene regulation pattern after GPR54 activation versus bradykinin B2 receptor
    Study

    n: not reported in source

    MDA-MB-435S cells expressing GPR54
    Comparator
    bradykinin B2 receptor activation
    Outcome group
    Receptor activity and mechanism · Cancer
    Studied dose
    Dose not stated · 25 hAs given in this study.

    Source sentences

    Summary
    Comparison with the bradykinin B(2) receptor revealed a distinct pattern of gene regulation despite a common coupling to the G(q/11) class of G-proteins.
    1 context sentence
    Summary · context
    To investigate the intracellular mechanisms involved in the reduction of the metastatic potential of MDA-MB-435S cells expressing GPR54, a time course stimulation by kisspeptin-10 over a period of 25 h was performed using cDNA microarrays.
  2. 02LabIn vitro (cells)Mechanism

    In MDA-MB-435S cells expressing GPR54, kisspeptin‑10 up-regulated several proapoptotic genes.

    In plain wordsIn cells, kisspeptin‑10 switched on several genes that promote cell death.

    Outcome
    IncreaseProapoptotic gene expression after GPR54 activation
    Study

    n: not reported in source

    MDA-MB-435S cells expressing GPR54
    Outcome group
    Tumor growth · Cancer
    Studied dose
    Dose not stated · 25 hAs given in this study.

    Source sentences

    Summary
    Among the genes specifically up-regulated by GPR54, we found several proapoptotic genes.
    1 context sentence
    Summary · context
    To investigate the intracellular mechanisms involved in the reduction of the metastatic potential of MDA-MB-435S cells expressing GPR54, a time course stimulation by kisspeptin-10 over a period of 25 h was performed using cDNA microarrays.
  3. 03LabIn vitro (cells)Mechanism

    In MDA-MB-435S cells expressing GPR54, GPR54 stimulation promoted apoptosis.

    In plain wordsIn cells, activating the kisspeptin receptor increased cell death.

    Outcome
    IncreaseApoptosis after GPR54 stimulation
    Study

    n: not reported in source

    MDA-MB-435S cells expressing GPR54
    Outcome group
    Tumor growth · Cancer
    Studied dose
    Dose not stated · 25 hAs given in this study.

    Source sentences

    Summary
    Stimulation of GPR54 promoted apoptosis
    1 context sentence
    Summary · context
    To investigate the intracellular mechanisms involved in the reduction of the metastatic potential of MDA-MB-435S cells expressing GPR54, a time course stimulation by kisspeptin-10 over a period of 25 h was performed using cDNA microarrays.

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. 04LabNot a test of Kisspeptin-10 aloneIn vitro (cells)Mechanism

    In cells stimulated through GPR54, inhibitors of PLC and PK-C abolished the transcriptional regulation of all tested genes.

    In plain wordsIn cells, blocking PLC or PK-C stopped the gene changes caused by GPR54 activation.

    Outcome
    DecreaseEffect of PLC and PK-C inhibitors on GPR54-induced gene regulation
    Study

    n: not reported in source

    MDA-MB-435S cells expressing GPR54
    Outcome group
    Receptor activity and mechanism · Cancer

    Source sentences

    Summary
    Inhibitors of PLC and PK-C abolished the transcriptional regulation of all tested genes
    1 context sentence
    Summary · context
    To investigate the intracellular mechanisms involved in the reduction of the metastatic potential of MDA-MB-435S cells expressing GPR54, a time course stimulation by kisspeptin-10 over a period of 25 h was performed using cDNA microarrays.

    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. 05LabNot a test of Kisspeptin-10 aloneIn vitro (cells)Mechanism

    In cells stimulated through GPR54, an inhibitor of p42/44 affected a subset of genes controlled by both GPR54 and B(2).

    In plain wordsIn cells, blocking p42/44 changed only some of the gene changes caused by GPR54 activation.

    Outcome
    MixedEffect of p42/44 inhibitor on GPR54-induced gene regulation
    Study

    n: not reported in source

    MDA-MB-435S cells expressing GPR54
    Outcome group
    Receptor activity and mechanism · Cancer

    Source sentences

    Summary
    while an inhibitor of p42/44 affected a subset of genes controlled both by GPR54 and B(2).
    1 context sentence
    Summary · context
    To investigate the intracellular mechanisms involved in the reduction of the metastatic potential of MDA-MB-435S cells expressing GPR54, a time course stimulation by kisspeptin-10 over a period of 25 h was performed using cDNA microarrays.

    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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