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Study · Animal study (in vivo) · 2022

3 results

Neuroendocrine Regulation of Stress-Induced T Cell Dysfunction during Lung Cancer Immunosurveillance via the Kisspeptin/GPR54 Signaling Pathway.

Zhang S, Yu F, Che A, Tan B, Huang C, Chen Y, Liu X, Huang Q, Zhang W, Ma C, Qian M, Liu M, Qin J, Du B

Advanced science (Weinheim, Baden-Wurttemberg, Germany)27 Feb 2022Cited by 30 (Europe PMC)

PMID35224894 (opens in a new tab)PMCIDPMC9069377 (opens in a new tab)DOI10.1002/advs.202104132 (opens in a new tab)PepBankPUB-35224894
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Summary

Emerging evidence suggests that physiological distress is highly correlated with cancer incidence and mortality. However, the mechanisms underlying psychological challenges-mediated tumor immune evasion are not systematically explored. Here, it is demonstrated that acute restraint (AR) increases the level of the plasma neuropeptide hormones, kisspeptin, and the expression levels of its receptor, Gpr54, in the hypothalamus, splenic and tumor-infiltrating T cells, suggesting a correlation between the neuroendocrine system and tumor microenvironment. Accordingly, administration of kisspeptin-10 significantly impairs T cell function, whereas knockout of Gpr54 in T cells inhibits lung tumor progression by suppressing T cell dysfunction and exhaustion with or without AR. In addition, Gpr54 defective OT-1 T cells show superior antitumor activity against OVA peptide-positive tumors. Mechanistically, ERK5-mediated NR4A1 activation is found to be essential for kisspeptin/GPR54-facilitated T cell dysfunction. Meanwhile, pharmacological inhibition of ERK5 signaling by XMD8-92 significantly reduces the tumor growth by enhancing CD8+ T cell antitumor function. Furthermore, depletion of GPR54 or ERK5 by CRISPR/Cas9 in CAR T cells intensifies the antitumor responses to both PSMA+ and CD19+ tumor cells, while eliminating T cell exhaustion. Taken together, these results indicate that kisspeptin/GPR54 signaling plays a nonredundant role in the stress-induced tumor immune evasion.
CC BYText from Europe PMC. Highlighted sentences are the source of results.

Results from this study3

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

  1. 01AnimalAnimal study (in vivo)Mechanism

    Administration of kisspeptin‑10 significantly impaired T cell function in a lung cancer immunosurveillance model.

    In plain wordsIn the study animals, giving kisspeptin‑10 weakened T cell function.

    Peptide
    Kisspeptin-10
    Outcome
    DecreaseT cell function
    Study

    n: not reported in source

    Outcome group
    Immune response · Immune and inflammation
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Accordingly, administration of kisspeptin-10 significantly impairs T cell function

Natural levels measured1

These results measure the body's own peptide. Nobody was given the peptide. They are not evidence about taking it. They are left out of key results, evidence counts and charts.

  1. 02AnimalEndogenous levelAnimal study (in vivo)Mechanism

    Acute restraint stress increased plasma levels of the neuropeptide hormone kisspeptin.

    In plain wordsIn the study animals, acute restraint stress raised the body's own kisspeptin levels in blood.

    Peptide
    Kisspeptin-10
    Outcome
    IncreasePlasma kisspeptin after acute restraint
    Study

    n: not reported in source

    Outcome group
    Stress hormones · Endocrine and hormones

    Source sentences

    Summary
    Here, it is demonstrated that acute restraint (AR) increases the level of the plasma neuropeptide hormones, kisspeptin, and the expression levels of its receptor, Gpr54, in the hypothalamus, splenic and tumor-infiltrating T cells, suggesting a correlation between the neuroendocrine system and tumor microenvironment.

    This result measures the body's own Kisspeptin-10. Nobody was given the peptide. It is not evidence about taking it.

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. 03AnimalNot a test of Kisspeptin-10 aloneAnimal study (in vivo)Efficacy outcome

    Knockout of the kisspeptin receptor Gpr54 in T cells inhibited lung tumor progression, with or without acute restraint. This tests the receptor, not administered kisspeptin‑10.

    In plain wordsIn the study animals, removing the kisspeptin receptor from T cells slowed lung tumor growth.

    Peptide
    Kisspeptin-10
    Outcome
    DecreaseLung tumor progression after Gpr54 knockout in T cells
    Study

    n: not reported in source

    Outcome group
    Tumor growth · Cancer

    Source sentences

    Summary
    whereas knockout of Gpr54 in T cells inhibits lung tumor progression by suppressing T cell dysfunction and exhaustion with or without AR.

    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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