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Study · In vitro (cells) · 2023

2 results

Kisspeptin-mediated improvement of sensitivity to BRAF inhibitors in vemurafenib-resistant melanoma cells.

Guzzetti C, Corno C, Vergani E, Mirra L, Ciusani E, Rodolfo M, Perego P, Beretta GL

Frontiers in oncology18 Sept 2023Cited by 5 (Europe PMC)

Summary

Metastatic dissemination is still one of the major causes of death of melanoma's patients. KiSS1 is a metastasis suppressor originally identified in melanoma cells, known to play an important physiological role in mammals' development and puberty. It has been previously shown that expression of KiSS1 could be increased in lung cancer cells using epigenetic agents, and that KiSS1 could have a pro-apoptotic action in combination with cisplatin. Thus, the aim of the present study was to examine in human melanoma vemurafenib sensitive- and -resistant BRAF mutant cells characterized by different mutational profiles and KiSS1, KiSS1 receptor and KiSS1 drug-induced release, if peptides derived from KiSS1 cleavage, i.e., kisspeptin 54, could increase the sensitivity to vemurafenib of human melanoma, using cellular, molecular and biochemical approaches. We found that kisspeptin 54 increases vemurafenib pro-apoptotic activity in a statistically significant manner, also in drug resistant cellular models. The efficacy of the combination appears to reflect the intrinsic susceptibility of each cell line to PLX4032-induced apoptosis, together with the different mutational profile as well as perturbation of proteins regulating the apoptotic pathway, The results presented here highlight the possibility to exploit KiSS1 to modulate the apoptotic response to therapeutically relevant agents, suggesting a multitasking function of this metastasis suppressor.
CC BYText from Europe PMC. Highlighted sentences are the source of results.

Results from this study2

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

  1. 01LabIn vitro (cells)Efficacy outcome

    In vemurafenib-sensitive human BRAF-mutant melanoma cells, kisspeptin‑54 significantly increased the pro-apoptotic activity of vemurafenib.

    In plain wordsIn melanoma cells, kisspeptin‑54 added to vemurafenib increased cell death more than vemurafenib alone.

    Outcome
    IncreaseVemurafenib pro-apoptotic activity
    Study

    humann: not reported in source

    human BRAF-mutant melanoma cells, vemurafenib-sensitive
    Comparator
    Vemurafenib alone
    Outcome group
    Tumor growth · Cancer
    Studied dose
    Dose not stated

    Source sentences

    Summary
    kisspeptin 54 increases vemurafenib pro-apoptotic activity in a statistically significant manner, also in drug resistant cellular models.
    1 context sentence
    Summary · context
    human melanoma vemurafenib sensitive- and -resistant BRAF mutant cells characterized by different mutational profiles and KiSS1, KiSS1 receptor and KiSS1 drug-induced release, if peptides derived from KiSS1 cleavage, i.e., kisspeptin 54, could increase the sensitivity to vemurafenib of human melanoma, using cellular, molecular and biochemical approaches
  2. 02LabIn vitro (cells)Efficacy outcome

    In vemurafenib-resistant human BRAF-mutant melanoma cell models, kisspeptin‑54 significantly increased the pro-apoptotic activity of vemurafenib.

    In plain wordsIn drug-resistant melanoma cells, kisspeptin‑54 added to vemurafenib increased cell death more than vemurafenib alone.

    Outcome
    IncreaseVemurafenib pro-apoptotic activity in resistant cells
    Study

    humann: not reported in source

    human BRAF-mutant melanoma cells, vemurafenib-resistant
    Comparator
    Vemurafenib alone
    Outcome group
    Tumor growth · Cancer
    Studied dose
    Dose not stated

    Source sentences

    Summary
    We found that kisspeptin 54 increases vemurafenib pro-apoptotic activity in a statistically significant manner, also in drug resistant cellular models.
    1 context sentence
    Summary · context
    human melanoma vemurafenib sensitive- and -resistant BRAF mutant cells characterized by different mutational profiles and KiSS1, KiSS1 receptor and KiSS1 drug-induced release, if peptides derived from KiSS1 cleavage, i.e., kisspeptin 54, could increase the sensitivity to vemurafenib of human melanoma, using cellular, molecular and biochemical approaches

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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

    13 Oct 2026, 21:44 UTC

    Study results updated

  2. Version 1

    13 Oct 2026, 16:31 UTC

    First added · source update from Europe PMC

Subjects

Terms as the source lists them.

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