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Study · In vitro (cells) · 2026

4 results

Integrated transcriptomics and miRNA-mRNA network analysis reveals Kisspeptin-10 mediated regulation of EMT and apoptosis in glioblastoma.

Shah H, Mohan AM, Shah R, Mehta D, Ramachandran AV, Pandya P

Computational biology and chemistry10 Dec 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 study4

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

  1. 01LabIn vitro (cells)Mechanism

    In glioblastoma cells, in-vitro validation supported a modulatory effect of Kisspeptin‑10 on EMT markers; the direction is not stated.

    In plain wordsIn glioblastoma cells, Kisspeptin‑10 changed markers of cell spread, but the abstract does not give the direction.

    Outcome
    Direction not reportedEMT markers after Kisspeptin-10
    Study

    humann: not reported in source

    Glioblastoma cells
    Outcome group
    Receptor activity and mechanism · Cancer
    Studied dose
    Dose not stated

    Source sentences

    Summary
    In-vitro validation further supported the modulatory effects of Kisspeptin-10 on EMT and apoptosis markers in GB cells.
    1 context sentence
    Summary · context
    This study aimed to investigate the regulatory effects of Kisspeptin-10 on epithelial-mesenchymal transition (EMT) and apoptosis in GB by integrating transcriptomic profiling, network analysis, and in-vitro validation.
  2. 02LabIn vitro (cells)Mechanism

    In glioblastoma cells, in-vitro validation supported a modulatory effect of Kisspeptin‑10 on apoptosis markers; the direction is not stated.

    In plain wordsIn glioblastoma cells, Kisspeptin‑10 changed markers of cell death, but the abstract does not give the direction.

    Outcome
    Direction not reportedApoptosis markers after Kisspeptin-10
    Study

    humann: not reported in source

    Glioblastoma cells
    Outcome group
    Receptor activity and mechanism · Cancer
    Studied dose
    Dose not stated

    Source sentences

    Summary
    In-vitro validation further supported the modulatory effects of Kisspeptin-10 on EMT and apoptosis markers in GB cells.
    1 context sentence
    Summary · context
    This study aimed to investigate the regulatory effects of Kisspeptin-10 on epithelial-mesenchymal transition (EMT) and apoptosis in GB by integrating transcriptomic profiling, network analysis, and in-vitro validation.

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. 03Computer modelNot a test of Kisspeptin-10 aloneIn silicoMechanism

    Analysis of public GEO datasets identified 1401 differentially expressed genes in glioblastoma (859 upregulated, 542 downregulated), enriched in EMT, cell-cycle, extracellular matrix and apoptosis pathways.

    In plain wordsA computer analysis of public tumour data found 1401 genes that differ in glioblastoma, linked to cell spread and cell death pathways.

    Outcome
    Not applicableDifferentially expressed genes in glioblastoma
    Study

    humann: not reported in source

    Public GEO glioblastoma datasets
    Outcome group
    Receptor activity and mechanism · Cancer

    Measurements

    Differentially expressed genes
    1401 genes
    glioblastoma datasets
    Upregulated genes
    859 genes
    glioblastoma datasets
    Downregulated genes
    542 genes
    glioblastoma datasets

    Source sentences

    Summary
    A total of 1401 DEGs were identified, including 859 upregulated and 542 downregulated genes, enriched in pathways associated with EMT regulation, cell-cycle progression, extracellular matrix remodeling, and apoptosis.
    1 context sentence
    Summary · context
    This study aimed to investigate the regulatory effects of Kisspeptin-10 on epithelial-mesenchymal transition (EMT) and apoptosis in GB by integrating transcriptomic profiling, network analysis, and in-vitro validation.

    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. 04Computer modelNot a test of Kisspeptin-10 aloneIn silicoMechanism

    Network analysis identified CDK1, CDC20, JUN and FABP5 as hub genes and miR-200, miR-345 and miR-577 as key regulatory miRNAs linked to EMT and apoptotic signaling in glioblastoma.

    In plain wordsA computer analysis of public tumour data named hub genes and small regulatory RNAs linked to glioblastoma cell spread and cell death.

    Outcome
    Not applicableHub genes and regulatory miRNAs in glioblastoma
    Study

    humann: not reported in source

    Public GEO glioblastoma datasets
    Outcome group
    Receptor activity and mechanism · Cancer

    Source sentences

    Summary
    Hub genes such as CDK1, CDC20, JUN, and FABP5 were identified, while miR-200, miR-345, and miR-577 emerged as key regulatory miRNAs linked to EMT and apoptotic signaling.
    1 context sentence
    Summary · context
    This study aimed to investigate the regulatory effects of Kisspeptin-10 on epithelial-mesenchymal transition (EMT) and apoptosis in GB by integrating transcriptomic profiling, network analysis, and in-vitro validation.

    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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