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Study · In vitro (cells) · 2026

9 results

Deciphering protein-DNA interactions of KISS1 with transcription factors through molecular docking, molecular dynamics simulations, and gene expression analysis.

Shah H, Pillai P, Buch L, Ramachandran AV, Pandya P

Journal of biomolecular structure & dynamics5 Sept 2025Cited by 2 (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 study9

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

  1. 01LabIn vitro (cells)Activity measurement

    In MDA-MB-231 triple-negative breast cancer cells, Kisspeptin‑10 had an IC50 of 100.21 nM.

    In plain wordsIn breast cancer cells in the lab, Kisspeptin‑10 had an IC50 of 100.21 nM.

    Outcome
    Not applicableKisspeptin-10 IC50
    Study

    humann: not reported in source

    MDA-MB-231 cells
    Outcome group
    Receptor activity and mechanism · Cancer
    Studied dose
    Dose not stated

    Measurements

    IC50
    100.21 nM
    MDA-MB-231 cells

    Source sentences

    Summary
    Experimental validation in MDA-MB-231 cells treated with Kisspeptin-10 (IC50: 100.21 nM) showed upregulation of SP1, NMYC, CDX2, and GATA2, and downregulation of FLI1 and HDAC2.
  2. 02LabIn vitro (cells)Mechanism

    In MDA-MB-231 cells, Kisspeptin‑10 upregulated SP1.

    In plain wordsIn breast cancer cells in the lab, Kisspeptin‑10 raised the level of SP1.

    Outcome
    IncreaseSP1 expression
    Study

    humann: not reported in source

    MDA-MB-231 cells
    Outcome group
    Receptor activity and mechanism · Cancer
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Experimental validation in MDA-MB-231 cells treated with Kisspeptin-10 (IC50: 100.21 nM) showed upregulation of SP1, NMYC, CDX2, and GATA2, and downregulation of FLI1 and HDAC2.
  3. 03LabIn vitro (cells)Mechanism

    In MDA-MB-231 cells, Kisspeptin‑10 upregulated NMYC.

    In plain wordsIn breast cancer cells in the lab, Kisspeptin‑10 raised the level of NMYC.

    Outcome
    IncreaseNMYC expression
    Study

    humann: not reported in source

    MDA-MB-231 cells
    Outcome group
    Receptor activity and mechanism · Cancer
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Experimental validation in MDA-MB-231 cells treated with Kisspeptin-10 (IC50: 100.21 nM) showed upregulation of SP1, NMYC, CDX2, and GATA2, and downregulation of FLI1 and HDAC2.
  4. 04LabIn vitro (cells)Mechanism

    In MDA-MB-231 cells, Kisspeptin‑10 upregulated CDX2.

    In plain wordsIn breast cancer cells in the lab, Kisspeptin‑10 raised the level of CDX2.

    Outcome
    IncreaseCDX2 expression
    Study

    humann: not reported in source

    MDA-MB-231 cells
    Outcome group
    Receptor activity and mechanism · Cancer
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Experimental validation in MDA-MB-231 cells treated with Kisspeptin-10 (IC50: 100.21 nM) showed upregulation of SP1, NMYC, CDX2, and GATA2, and downregulation of FLI1 and HDAC2.
  5. 05LabIn vitro (cells)Mechanism

    In MDA-MB-231 cells, Kisspeptin‑10 upregulated GATA2.

    In plain wordsIn breast cancer cells in the lab, Kisspeptin‑10 raised the level of GATA2.

    Outcome
    IncreaseGATA2 expression
    Study

    humann: not reported in source

    MDA-MB-231 cells
    Outcome group
    Receptor activity and mechanism · Cancer
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Experimental validation in MDA-MB-231 cells treated with Kisspeptin-10 (IC50: 100.21 nM) showed upregulation of SP1, NMYC, CDX2, and GATA2, and downregulation of FLI1 and HDAC2.
  6. 06LabIn vitro (cells)Mechanism

    In MDA-MB-231 cells, Kisspeptin‑10 downregulated FLI1.

    In plain wordsIn breast cancer cells in the lab, Kisspeptin‑10 lowered the level of FLI1.

    Outcome
    DecreaseFLI1 expression
    Study

    humann: not reported in source

    MDA-MB-231 cells
    Outcome group
    Receptor activity and mechanism · Cancer
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Experimental validation in MDA-MB-231 cells treated with Kisspeptin-10 (IC50: 100.21 nM) showed upregulation of SP1, NMYC, CDX2, and GATA2, and downregulation of FLI1 and HDAC2.
  7. 07LabIn vitro (cells)Mechanism

    In MDA-MB-231 cells, Kisspeptin‑10 downregulated HDAC2.

    In plain wordsIn breast cancer cells in the lab, Kisspeptin‑10 lowered the level of HDAC2.

    Outcome
    DecreaseHDAC2 expression
    Study

    humann: not reported in source

    MDA-MB-231 cells
    Outcome group
    Receptor activity and mechanism · Cancer
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Experimental validation in MDA-MB-231 cells treated with Kisspeptin-10 (IC50: 100.21 nM) showed upregulation of SP1, NMYC, CDX2, and GATA2, and downregulation of FLI1 and HDAC2.

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. 08Computer modelNot a test of Kisspeptin-10 aloneIn silicoMechanism

    In docking, CDX2 showed the strongest binding to KISS1 DNA, followed by HDAC2, GATA2, NMYC, SP1 and FLI1.

    In plain wordsA computer docking study found the protein CDX2 bound KISS1 gene DNA most strongly of the six proteins tested.

    Outcome
    Not applicableDocking of KISS1 DNA with transcription factors
    Study

    n: not reported in source

    HADDOCK docking of KISS1 DNA with transcription factors
    Outcome group
    Receptor activity and mechanism · Cancer

    Measurements

    HADDOCK score
    −144.2
    CDX2

    Source sentences

    Summary
    CDX2 showed the strongest binding (HADDOCK score: -144.2; buried surface area: 2526.5 Å2), followed by HDAC2, GATA2, NMYC, SP1, and FLI1.

    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. 09Computer modelNot a test of Kisspeptin-10 aloneIn silicoMechanism

    In 150-ns molecular dynamics simulations, the KISS1 DNA complexes with SP1, NMYC and CDX2 were stable, whereas FLI1 and GATA2 showed greater flexibility and unstable interactions.

    In plain wordsComputer simulations showed that KISS1 gene DNA formed stable complexes with SP1, NMYC and CDX2, but not with FLI1 and GATA2.

    Outcome
    Not applicableStability of KISS1 DNA complexes
    Study

    n: not reported in source

    150-ns molecular dynamics of KISS1 DNA complexes
    Outcome group
    Receptor activity and mechanism · Cancer

    Source sentences

    Summary
    Molecular dynamics simulations (150 ns) revealed stable complexes for SP1, NMYC, and CDX2 with low RMSD (2.1-2.7 Å), compact Rg (∼21.0 Å), and stable hydrogen bonding (5-9 bonds).
    1 context sentence
    Summary · context
    In contrast, FLI1 and GATA2 showed greater flexibility and unstable interactions.

    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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