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Study · Not a test of the peptide alone · 2019

1 result

CYT997(Lexibulin) induces apoptosis and autophagy through the activation of mutually reinforced ER stress and ROS in osteosarcoma.

Wang Z, Yin F, Xu J, Zhang T, Wang G, Mao M, Wang Z, Sun W, Han J, Yang M, Jiang Y, Hua Y, Cai Z

Journal of experimental & clinical cancer research : CR31 Jan 2019Cited by 89 (Europe PMC)

PMID30704503 (opens in a new tab)PMCIDPMC6357486 (opens in a new tab)DOI10.1186/s13046-019-1047-9 (opens in a new tab)PepBankPUB-30704503
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Summary

BackgroundOsteosarcoma (OS) is a common malignant cancer in children and adolescents and has a cure rate that has not improved in the last two decades. CYT997 (lexibulin) is a novel potent microtubule-targeting agent with various anticancer activities, such as proliferation inhibition, vascular disruption, and cell cycle arrest and apoptosis induction, in multiple cancers. However, the direct cytotoxic mechanisms of CYT997 have not yet been fully characterized.MethodsWe evaluated apoptosis and autophagy in human osteosarcomas after treatment with CYT997 and investigated the underlying mechanisms. To explore relationships, we used the reactive oxygen species (ROS) scavenger N-acetyl cysteine (NAC), PERK inhibitor GSK2606414, ERO1 inhibitor EN460 and mitochondrial targeted protection peptide elamipretide. BALB/c-nu mice were inoculated with 143B tumor cells to investigate the in vivo effect of CYT997.ResultsWe explored the efficacy and mechanism of CYT997 in osteosarcoma (OS) in vitro and in vivo and demonstrated that CYT997 potently suppresses cell viability and induces apoptosis and autophagy. CYT997 triggered production of ROS and exerted lethal effects via endoplasmic reticulum (ER) stress in OS cells. NAC attenuated these effects. The PERK inhibitor GSK2606414, which can block the ER stress pathway, reduced ROS production and enhanced cell viability. Moreover, activation of ERO1 in the ER stress pathway was responsible for inducing ROS production. ROS produced by the mitochondrial pathway also aggravate ER stress. Protection of mitochondria can reduce apoptosis and autophagy. Finally, CYT997 prominently reduced tumor growth in vivo.ConclusionsThis study suggests that CYT997 induces apoptosis and autophagy in OS cells by triggering mutually enhanced ER stress and ROS and may thus be a promising agent against OS.
CC BYText from Europe PMC. Highlighted sentences are the source of results.

Results from this study1

No result from this study comes from a test of the peptide.

Studies that did not test the peptide alone1

In this study, Elamipretide (SS-31) 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 Elamipretide (SS-31).

  1. 01LabNot a test of Elamipretide (SS-31) aloneIn vitro (cells)Mechanism

    In osteosarcoma cells, mitochondrial protection (tested with elamipretide) reduced apoptosis and autophagy induced by CYT997.

    In plain wordsIn osteosarcoma cells, protecting mitochondria reduced cell death and autophagy caused by the drug CYT997.

    Peptide
    Elamipretide (SS-31)
    Outcome
    DecreaseCYT997-induced apoptosis and autophagy with mitochondrial protection
    Study

    humann: not reported in source

    Human osteosarcoma cells treated with CYT997
    Outcome group
    Tumor growth · Cancer

    Source sentences

    Summary
    Protection of mitochondria can reduce apoptosis and autophagy.
    1 context sentence
    Summary · context
    mitochondrial targeted protection peptide elamipretide.

    In this study, Elamipretide (SS-31) 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 Elamipretide (SS-31).

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, 08:19 UTC

    Study results updated

  2. Version 1

    9 Oct 2026, 02:47 UTC

    First added · source update from Europe PMC

Subjects

Terms as the source lists them.

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