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Study · In vitro (cells) · 2026

6 results

Exogenous Kisspeptin-10 inhibits ovarian cancer progression through targeting the SP1-hTERT-ZEB1 regulatory axis.

Shah H, Thomas A, Pandya P

Cytotechnology11 Jun 2026

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 study6

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

  1. 01LabIn vitro (cells)Efficacy outcome

    In SKOV-3 ovarian cancer cells, Kisspeptin‑10 significantly inhibited proliferation in a dose-dependent manner, with a half-maximal inhibitory concentration of 72.28 nM.

    In plain wordsIn ovarian cancer cells in the lab, Kisspeptin‑10 slowed cell growth, and more so at higher doses.

    Outcome
    DecreaseSKOV-3 proliferation
    Study

    humann: not reported in source

    SKOV-3 ovarian cancer cells
    Outcome group
    Tumor growth · Cancer
    Studied dose
    Dose not stated

    Measurements

    IC50
    72.28 nM
    SKOV-3 cells

    Source sentences

    Summary
    KP-10 significantly inhibited SKOV-3 proliferation, migration, and invasion at a dose-dependent level with an IC₅₀ of 72.28 nM.
    1 context sentence
    Summary · context
    The current study aims to explore the influence of exogenous Kisspeptin-10 (KP-10) on the SP1-ZEB1-hTERT pathway in SKOV-3 ovarian cancer cell lines using both in vitro and computational techniques.
  2. 02LabIn vitro (cells)Efficacy outcome

    In SKOV-3 ovarian cancer cells, Kisspeptin‑10 significantly inhibited migration in a dose-dependent manner.

    In plain wordsIn ovarian cancer cells in the lab, Kisspeptin‑10 reduced cell movement, and more so at higher doses.

    Outcome
    DecreaseSKOV-3 migration
    Study

    humann: not reported in source

    SKOV-3 ovarian cancer cells
    Outcome group
    Tumor growth · Cancer
    Studied dose
    Dose not stated

    Source sentences

    Summary
    KP-10 significantly inhibited SKOV-3 proliferation, migration, and invasion at a dose-dependent level with an IC₅₀ of 72.28 nM.
    1 context sentence
    Summary · context
    The current study aims to explore the influence of exogenous Kisspeptin-10 (KP-10) on the SP1-ZEB1-hTERT pathway in SKOV-3 ovarian cancer cell lines using both in vitro and computational techniques.
  3. 03LabIn vitro (cells)Efficacy outcome

    In SKOV-3 ovarian cancer cells, Kisspeptin‑10 significantly inhibited invasion in a dose-dependent manner.

    In plain wordsIn ovarian cancer cells in the lab, Kisspeptin‑10 reduced cell invasion, and more so at higher doses.

    Outcome
    DecreaseSKOV-3 invasion
    Study

    humann: not reported in source

    SKOV-3 ovarian cancer cells
    Outcome group
    Tumor growth · Cancer
    Studied dose
    Dose not stated

    Source sentences

    Summary
    KP-10 significantly inhibited SKOV-3 proliferation, migration, and invasion at a dose-dependent level with an IC₅₀ of 72.28 nM.
    1 context sentence
    Summary · context
    The current study aims to explore the influence of exogenous Kisspeptin-10 (KP-10) on the SP1-ZEB1-hTERT pathway in SKOV-3 ovarian cancer cell lines using both in vitro and computational techniques.
  4. 04LabIn vitro (cells)Mechanism

    In SKOV-3 cells, Kisspeptin‑10 affected the regulation of the transcription factors SP1, CDX2, GATA2, FLI1 and ZEB1 and of hTERT expression; the direction is not stated.

    In plain wordsIn ovarian cancer cells in the lab, Kisspeptin‑10 changed the activity of several cancer-related genes.

    Outcome
    Direction not reportedTranscription factor and hTERT expression
    Study

    humann: not reported in source

    SKOV-3 ovarian cancer cells
    Outcome group
    Receptor activity and mechanism · Cancer
    Studied dose
    Dose not stated

    Source sentences

    Summary
    The molecular mechanisms showed the ability of KP-10 to affect the regulation of important transcriptional factors such as SP1, CDX2, GATA2, FLI1, and ZEB1 and hTERT expression, indicating telomerase-related oncogenic signaling modulation.
    1 context sentence
    Summary · context
    The current study aims to explore the influence of exogenous Kisspeptin-10 (KP-10) on the SP1-ZEB1-hTERT pathway in SKOV-3 ovarian cancer cell lines using both in vitro and computational techniques.
  5. 05LabIn vitro (cells)Mechanism

    In SKOV-3 cells, Kisspeptin‑10 influenced the expression of the tumor suppressive microRNAs miR-200, miR-345 and miR-577; the direction is not stated.

    In plain wordsIn ovarian cancer cells in the lab, Kisspeptin‑10 changed levels of small RNAs that restrain cancer spread.

    Outcome
    Direction not reportedTumor suppressive miRNA expression
    Study

    humann: not reported in source

    SKOV-3 ovarian cancer cells
    Outcome group
    Receptor activity and mechanism · Cancer
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Besides, KP-10 influenced the expression of tumor suppressive microRNAs, including miR-200, miR-345, and miR-577 which are known to inhibit epithelial-mesenchymal transition, invasion, and development of cancer.
    1 context sentence
    Summary · context
    The current study aims to explore the influence of exogenous Kisspeptin-10 (KP-10) on the SP1-ZEB1-hTERT pathway in SKOV-3 ovarian cancer cell lines using both in vitro and computational techniques.

Studies that did not test the peptide alone1

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. 06Computer modelNot a test of Kisspeptin-10 aloneIn silicoMechanism

    Bioinformatics analysis of the KISS1 promoter showed multiple binding sites for SP1, CDX2, GATA2 and FLI1, among others.

    In plain wordsA computer analysis of the KISS1 gene promoter found several binding sites for gene-control proteins.

    Outcome
    Not applicableKISS1 promoter transcription factor binding sites
    Study

    n: not reported in source

    KISS1 promoter sequence analysis
    Outcome group
    Receptor activity and mechanism · Cancer

    Source sentences

    Summary
    The bioinformatics analysis of the KISS1 promoter showed multiple binding sites of SP1, CDX2, GATA2, FLI1, among others, indicating the transcription network in KISS1 regulation.

    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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