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Study · Animal study (in vivo) · 2024

7 results

Humanin activates integrin αV-TGFβ axis and leads to glioblastoma progression.

Ha CP, Hua TNM, Vo VTA, Om J, Han S, Cha SK, Park KS, Jeong Y

Cell death & disease28 Jun 2024Cited by 7 (Europe PMC)

Summary

The role of mitochondria peptides in the spreading of glioblastoma remains poorly understood. In this study, we investigated the mechanism underlying intracranial glioblastoma progression. Our findings demonstrate that the mitochondria-derived peptide, humanin, plays a significant role in enhancing glioblastoma progression through the intratumoral activation of the integrin alpha V (ITGAV)-TGF beta (TGFβ) signaling axis. In glioblastoma tissues, humanin showed a significant upregulation in the tumor area compared to the corresponding normal region. Utilizing multiple in vitro pharmacological and genetic approaches, we observed that humanin activates the ITGAV pathway, leading to cellular attachment and filopodia formation. This process aids the subsequent migration and invasion of attached glioblastoma cells through intracellular TGFβR signaling activation. In addition, our in vivo orthotopic glioblastoma model provides further support for the pro-tumoral function of humanin. We observed a correlation between poor survival and aggressive invasiveness in the humanin-treated group, with noticeable tumor protrusions and induced angiogenesis compared to the control. Intriguingly, the in vivo effect of humanin on glioblastoma was significantly reduced by the treatment of TGFBR1 inhibitor. To strengthen these findings, public database analysis revealed a significant association between genes in the ITGAV-TGFβR axis and poor prognosis in glioblastoma patients. These results collectively highlight humanin as a pro-tumoral factor, making it a promising biological target for treating glioblastoma.
CC BYText from Europe PMC. Highlighted sentences are the source of results.

Results from this study7

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

  1. 01AnimalAnimal study (in vivo)Efficacy outcome

    In an orthotopic glioblastoma model, poor survival correlated with humanin treatment compared with control.

    In plain wordsIn an animal glioblastoma model, humanin treatment was linked to poorer survival than control.

    Peptide
    Humanin
    Outcome
    DecreaseSurvival in orthotopic glioblastoma model
    Study

    n: not reported in source

    Orthotopic glioblastoma model
    Comparator
    Control
    Outcome group
    Mortality · Cancer
    Studied dose
    Dose not stated

    Source sentences

    Summary
    In addition, our in vivo orthotopic glioblastoma model provides further support for the pro-tumoral function of humanin. We observed a correlation between poor survival and aggressive invasiveness in the humanin-treated group, with noticeable tumor protrusions and induced angiogenesis compared to the control.
  2. 02AnimalAnimal study (in vivo)Efficacy outcome

    In an orthotopic glioblastoma model, the humanin-treated group showed aggressive invasiveness with noticeable tumor protrusions compared with control.

    In plain wordsIn an animal glioblastoma model, humanin-treated tumors were more invasive and had more protrusions than control.

    Peptide
    Humanin
    Outcome
    IncreaseTumor invasiveness and protrusions
    Study

    n: not reported in source

    Orthotopic glioblastoma model
    Comparator
    Control
    Outcome group
    Tumor growth · Cancer
    Studied dose
    Dose not stated

    Source sentences

    Summary
    In addition, our in vivo orthotopic glioblastoma model provides further support for the pro-tumoral function of humanin. We observed a correlation between poor survival and aggressive invasiveness in the humanin-treated group, with noticeable tumor protrusions and induced angiogenesis compared to the control.
  3. 03AnimalAnimal study (in vivo)Mechanism

    In an orthotopic glioblastoma model, humanin treatment induced angiogenesis compared with control.

    In plain wordsIn an animal glioblastoma model, humanin treatment led to more new blood vessel growth in tumors than control.

    Peptide
    Humanin
    Outcome
    IncreaseTumor angiogenesis
    Study

    n: not reported in source

    Orthotopic glioblastoma model
    Comparator
    Control
    Outcome group
    Tumor growth · Cancer
    Studied dose
    Dose not stated

    Source sentences

    Summary
    In addition, our in vivo orthotopic glioblastoma model provides further support for the pro-tumoral function of humanin. We observed a correlation between poor survival and aggressive invasiveness in the humanin-treated group, with noticeable tumor protrusions and induced angiogenesis compared to the control.
  4. 04LabIn vitro (cells)Mechanism

    In glioblastoma cells, humanin activated the ITGAV pathway, which led to cellular attachment and filopodia formation.

    In plain wordsIn cells, humanin switched on the ITGAV pathway, and the glioblastoma cells attached more and formed filopodia.

    Peptide
    Humanin
    Outcome
    IncreaseITGAV pathway activation, cell attachment and filopodia formation
    Study

    n: not reported in source

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

    Source sentences

    Summary
    Utilizing multiple in vitro pharmacological and genetic approaches, we observed that humanin activates the ITGAV pathway, leading to cellular attachment and filopodia formation.
  5. 05LabIn vitro (cells)Mechanism

    In attached glioblastoma cells, humanin-driven signalling aided migration and invasion through intracellular TGFBR signaling activation.

    In plain wordsIn cells, humanin helped attached glioblastoma cells to migrate and invade, through TGFBR signalling.

    Peptide
    Humanin
    Outcome
    IncreaseMigration and invasion of attached glioblastoma cells
    Study

    n: not reported in source

    Glioblastoma cells
    Outcome group
    Tumor growth · Cancer
    Studied dose
    Dose not stated

    Source sentences

    Summary
    This process aids the subsequent migration and invasion of attached glioblastoma cells through intracellular TGFβR signaling activation.

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. 06HumanEndogenous levelObservational studyOther

    In glioblastoma tissues, humanin was upregulated in the tumor area compared with the corresponding normal region.

    In plain wordsIn glioblastoma tissue samples, the body's own humanin was higher in the tumor area than in the matching normal region.

    Peptide
    Humanin
    Outcome
    IncreaseHumanin level in glioblastoma tissue
    Study

    n: not reported in source

    Comparator
    Corresponding normal region
    Outcome group
    Tumor growth · Cancer

    Source sentences

    Summary
    In glioblastoma tissues, humanin showed a significant upregulation in the tumor area compared to the corresponding normal region.

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

Studies that did not test the peptide alone1

In this study, Humanin 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 Humanin.

  1. 07AnimalNot a test of Humanin aloneAnimal study (in vivo)Mechanism

    In an in vivo glioblastoma model, treatment with a TGFBR1 inhibitor significantly reduced the effect of humanin on glioblastoma.

    In plain wordsIn an animal glioblastoma model, a TGFBR1 inhibitor reduced the effect that humanin had on the tumor.

    Peptide
    Humanin
    Outcome
    DecreaseHumanin effect on glioblastoma with TGFBR1 inhibitor
    Study

    n: not reported in source

    Orthotopic glioblastoma model
    Outcome group
    Tumor growth · Cancer

    Source sentences

    Summary
    Intriguingly, the in vivo effect of humanin on glioblastoma was significantly reduced by the treatment of TGFBR1 inhibitor.

    In this study, Humanin 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 Humanin.

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

    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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