Skip to content

Study · In vitro (cells) · 2022

5 results

Lack of Oestrogen Receptor Expression in Breast Cancer Cells Does Not Correlate with Kisspeptin Signalling and Migration.

Azubuike UF, Newton CL, van den Bout I

International journal of molecular sciences6 Aug 2022Cited by 1 (Europe PMC)

PMID35955878 (opens in a new tab)PMCIDPMC9368979 (opens in a new tab)DOI10.3390/ijms23158744 (opens in a new tab)PepBankPUB-35955878
Download PDFPubMedAsk about this study
Jump to 5 results

Summary

Kisspeptin is an anti-metastatic mediator in many cancer types, acting through its receptor, KISS1R. However, controversy remains regarding its role in breast cancer since both pro- and anti-metastatic roles have been ascribed to it. In KISS1R overexpressing triple-negative breast cancer (TNBC) cells, stimulation has been associated with increased invasion and MMP-9 expression, leading to the suggestion that hormone receptor status determines the metastatic effects of kisspeptin. To assess the veracity of this claim, we compared endogenous KISS1R signalling and physiological output in the hormone receptor-negative MDA-MB-231 and BT-20 cell lines after KP-10 (shortest active kisspeptin peptide) stimulation. MDA-MB-231 cells are metastatic when implanted in mice while BT-20 are not and remain epithelial-like. We show that both cell lines express KISS1R mRNA and respond to KP-10 by elevating calcium mobilisation. However, KP-10 stimulation induced migration of MDA-MB-231, but not BT-20 cells, in a calcium-dependent manner. Moreover, only BT-20 cells responded to KP-10 by increasing ERK phosphorylation in a β-arrestin-dependent manner. Interestingly, both cell lines displayed different complements of β-arrestin 1 and 2 expression. Overall, our data shows that, in TNBC, it is not universally true that kisspeptin/KISS1R stimulate migration or pro-metastatic behaviour, as divergent responses were observed in the two TNBC lines tested. Whether this divergence is related to the observed differences in β-arrestin complements warrants further investigation and may enable further stratification of the ability of kisspeptin to influence breast tumour behaviour.
CC BYText from Europe PMC. Highlighted sentences are the source of results.

Results from this study5

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

  1. 01LabIn vitro (cells)Mechanism

    In MDA-MB-231 and BT-20 breast cancer cells, KP-10 elevated calcium mobilisation.

    In plain wordsIn cells, KP-10 raised calcium signals in both breast cancer cell lines.

    Peptide
    Kisspeptin-10
    Outcome
    IncreaseCalcium mobilisation after KP-10 in MDA-MB-231 and BT-20 cells
    Study

    n: not reported in source

    MDA-MB-231 and BT-20 triple-negative breast cancer cell lines
    Outcome group
    Receptor activity and mechanism · Cancer
    Studied dose
    Dose not stated

    Source sentences

    Summary
    respond to KP-10 by elevating calcium mobilisation.
    1 context sentence
    Summary · context
    To assess the veracity of this claim, we compared endogenous KISS1R signalling and physiological output in the hormone receptor-negative MDA-MB-231 and BT-20 cell lines after KP-10 (shortest active kisspeptin peptide) stimulation.
  2. 02LabIn vitro (cells)Efficacy outcome

    In MDA-MB-231 breast cancer cells, KP-10 induced migration in a calcium-dependent manner.

    In plain wordsIn cells, KP-10 made MDA-MB-231 breast cancer cells migrate more.

    Peptide
    Kisspeptin-10
    Outcome
    IncreaseMigration of MDA-MB-231 cells after KP-10
    Study

    n: not reported in source

    MDA-MB-231 and BT-20 triple-negative breast cancer cell lines
    Outcome group
    Tumor growth · Cancer
    Studied dose
    Dose not stated

    Source sentences

    Summary
    However, KP-10 stimulation induced migration of MDA-MB-231, but not BT-20 cells, in a calcium-dependent manner.
    1 context sentence
    Summary · context
    To assess the veracity of this claim, we compared endogenous KISS1R signalling and physiological output in the hormone receptor-negative MDA-MB-231 and BT-20 cell lines after KP-10 (shortest active kisspeptin peptide) stimulation.
  3. 03LabIn vitro (cells)Efficacy outcome

    In BT-20 breast cancer cells, KP-10 did not induce migration.

    In plain wordsIn cells, KP-10 did not make BT-20 breast cancer cells migrate.

    Peptide
    Kisspeptin-10
    Outcome
    No significant changeMigration of BT-20 cells after KP-10
    Study

    n: not reported in source

    MDA-MB-231 and BT-20 triple-negative breast cancer cell lines
    Outcome group
    Tumor growth · Cancer
    Studied dose
    Dose not stated

    Source sentences

    Summary
    However, KP-10 stimulation induced migration of MDA-MB-231, but not BT-20 cells, in a calcium-dependent manner.
    1 context sentence
    Summary · context
    To assess the veracity of this claim, we compared endogenous KISS1R signalling and physiological output in the hormone receptor-negative MDA-MB-231 and BT-20 cell lines after KP-10 (shortest active kisspeptin peptide) stimulation.
  4. 04LabIn vitro (cells)Mechanism

    In BT-20 breast cancer cells, KP-10 increased ERK phosphorylation in a β-arrestin-dependent manner.

    In plain wordsIn cells, KP-10 increased ERK signalling in BT-20 breast cancer cells.

    Peptide
    Kisspeptin-10
    Outcome
    IncreaseERK phosphorylation in BT-20 cells after KP-10
    Study

    n: not reported in source

    MDA-MB-231 and BT-20 triple-negative breast cancer cell lines
    Outcome group
    Receptor activity and mechanism · Cancer
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Moreover, only BT-20 cells responded to KP-10 by increasing ERK phosphorylation in a β-arrestin-dependent manner.
    1 context sentence
    Summary · context
    To assess the veracity of this claim, we compared endogenous KISS1R signalling and physiological output in the hormone receptor-negative MDA-MB-231 and BT-20 cell lines after KP-10 (shortest active kisspeptin peptide) stimulation.
  5. 05LabIn vitro (cells)Mechanism

    In MDA-MB-231 breast cancer cells, KP-10 did not increase ERK phosphorylation.

    In plain wordsIn cells, KP-10 did not increase ERK signalling in MDA-MB-231 breast cancer cells.

    Peptide
    Kisspeptin-10
    Outcome
    No significant changeERK phosphorylation in MDA-MB-231 cells after KP-10
    Study

    n: not reported in source

    MDA-MB-231 and BT-20 triple-negative breast cancer cell lines
    Outcome group
    Receptor activity and mechanism · Cancer
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Moreover, only BT-20 cells responded to KP-10 by increasing ERK phosphorylation in a β-arrestin-dependent manner.
    1 context sentence
    Summary · context
    To assess the veracity of this claim, we compared endogenous KISS1R signalling and physiological output in the hormone receptor-negative MDA-MB-231 and BT-20 cell lines after KP-10 (shortest active kisspeptin peptide) stimulation.

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.