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Study · In vitro (cells) · 2015

9 results

The oncolytic peptide LTX-315 kills cancer cells through Bax/Bak-regulated mitochondrial membrane permeabilization.

Zhou H, Forveille S, Sauvat A, Sica V, Izzo V, Durand S, Müller K, Liu P, Zitvogel L, Rekdal Ø, Kepp O, Kroemer G

Oncotarget1 Sept 2015Cited by 46 (Europe PMC)

PMID26378049 (opens in a new tab)PMCIDPMC4694939 (opens in a new tab)DOI10.18632/oncotarget.5613 (opens in a new tab)PepBankPUB-26378049
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Summary

LTX-315 has been developed as an amphipathic cationic peptide that kills cancer cells. Here, we investigated the putative involvement of mitochondria in the cytotoxic action of LTX-315. Subcellular fractionation of LTX-315-treated cells, followed by mass spectrometric quantification, revealed that the agent was enriched in mitochondria. LTX-315 caused an immediate arrest of mitochondrial respiration without any major uncoupling effect. Accordingly, LTX-315 disrupted the mitochondrial network, dissipated the mitochondrial inner transmembrane potential, and caused the release of mitochondrial intermembrane proteins into the cytosol. LTX-315 was relatively inefficient in stimulating mitophagy. Cells lacking the two pro-apoptotic multidomain proteins from the BCL-2 family, BAX and BAK, were less susceptible to LTX-315-mediated killing. Moreover, cells engineered to lose their mitochondria (by transfection with Parkin combined with treatment with a protonophore causing mitophagy) were relatively resistant against LTX-315, underscoring the importance of this organelle for LTX-315-mediated cytotoxicity. Altogether, these results support the notion that LTX-315 kills cancer cells by virtue of its capacity to permeabilize mitochondrial membranes.
CC BYText from Europe PMC. Highlighted sentences are the source of results.

Results from this study9

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

  1. 01LabIn vitro (cells)Mechanism

    In treated cells, LTX‑315 was enriched in mitochondria.

    In plain wordsIn cells, LTX‑315 accumulated in mitochondria.

    Peptide
    LTX-315
    Outcome
    IncreaseMitochondrial enrichment
    Study

    n: not reported in source

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

    Source sentences

    Summary
    Subcellular fractionation of LTX-315-treated cells, followed by mass spectrometric quantification, revealed that the agent was enriched in mitochondria.
  2. 02LabIn vitro (cells)Mechanism

    In cells, LTX‑315 caused immediate arrest of mitochondrial respiration.

    In plain wordsIn cells, LTX‑315 immediately stopped mitochondrial respiration.

    Peptide
    LTX-315
    Outcome
    DecreaseMitochondrial respiration
    Study

    n: not reported in source

    cancer cells
    Outcome group
    Mitochondrial function · Cancer
    Studied dose
    Dose not stated

    Source sentences

    Summary
    LTX-315 caused an immediate arrest of mitochondrial respiration without any major uncoupling effect.
  3. 03LabIn vitro (cells)Mechanism

    In cells, LTX‑315 arrested mitochondrial respiration without a major uncoupling effect.

    In plain wordsIn cells, LTX‑315 stopped mitochondrial respiration without a major uncoupling effect.

    Peptide
    LTX-315
    Outcome
    Not applicableMitochondrial uncoupling
    Study

    n: not reported in source

    cancer cells
    Outcome group
    Mitochondrial function · Cancer
    Studied dose
    Dose not stated

    Source sentences

    Summary
    LTX-315 caused an immediate arrest of mitochondrial respiration without any major uncoupling effect.
  4. 04LabIn vitro (cells)Mechanism

    In cells, LTX‑315 disrupted the mitochondrial network.

    In plain wordsIn cells, LTX‑315 disrupted the mitochondrial network.

    Peptide
    LTX-315
    Outcome
    Not applicableMitochondrial network disruption
    Study

    n: not reported in source

    cancer cells
    Outcome group
    Mitochondrial function · Cancer
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Accordingly, LTX-315 disrupted the mitochondrial network, dissipated the mitochondrial inner transmembrane potential, and caused the release of mitochondrial intermembrane proteins into the cytosol.
  5. 05LabIn vitro (cells)Mechanism

    In cells, LTX‑315 dissipated the mitochondrial inner transmembrane potential.

    In plain wordsIn cells, LTX‑315 dissipated the electrical potential across the inner mitochondrial membrane.

    Peptide
    LTX-315
    Outcome
    DecreaseMitochondrial transmembrane potential
    Study

    n: not reported in source

    cancer cells
    Outcome group
    Mitochondrial function · Cancer
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Accordingly, LTX-315 disrupted the mitochondrial network, dissipated the mitochondrial inner transmembrane potential, and caused the release of mitochondrial intermembrane proteins into the cytosol.
  6. 06LabIn vitro (cells)Mechanism

    In cells, LTX‑315 released mitochondrial intermembrane proteins into the cytosol.

    In plain wordsIn cells, LTX‑315 released proteins from between mitochondrial membranes into the surrounding cell fluid.

    Peptide
    LTX-315
    Outcome
    IncreaseMitochondrial protein release
    Study

    n: not reported in source

    cancer cells
    Outcome group
    Mitochondrial function · Cancer
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Accordingly, LTX-315 disrupted the mitochondrial network, dissipated the mitochondrial inner transmembrane potential, and caused the release of mitochondrial intermembrane proteins into the cytosol.
  7. 07LabIn vitro (cells)Mechanism

    In cells, LTX‑315 was relatively inefficient in stimulating mitophagy.

    In plain wordsIn cells, LTX‑315 was relatively inefficient in stimulating mitochondrial removal.

    Peptide
    LTX-315
    Outcome
    Not applicableMitophagy stimulation
    Study

    n: not reported in source

    cancer cells
    Outcome group
    Mitochondrial function · Cancer
    Studied dose
    Dose not stated

    Source sentences

    Summary
    LTX-315 was relatively inefficient in stimulating mitophagy.
  8. 08LabIn vitro (cells)Mechanism

    In cells lacking BAX and BAK, susceptibility to LTX‑315-mediated killing was lower.

    In plain wordsIn cells lacking BAX and BAK, LTX‑315 killed less readily than in cells with these proteins.

    Peptide
    LTX-315
    Outcome
    DecreaseKilling susceptibility without BAX and BAK
    Study

    n: not reported in source

    cancer cells
    Comparator
    cells with BAX and BAK
    Outcome group
    Receptor activity and mechanism · Cancer
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Cells lacking the two pro-apoptotic multidomain proteins from the BCL-2 family, BAX and BAK, were less susceptible to LTX-315-mediated killing.
  9. 09LabIn vitro (cells)Mechanism

    In cells engineered to lose mitochondria, susceptibility to LTX‑315-mediated killing was relatively low.

    In plain wordsIn cells engineered to lose mitochondria, resistance to LTX‑315 was higher than in cells retaining mitochondria.

    Peptide
    LTX-315
    Outcome
    DecreaseKilling susceptibility without mitochondria
    Study

    n: not reported in source

    cancer cells
    Comparator
    cells retaining mitochondria
    Outcome group
    Receptor activity and mechanism · Cancer
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Moreover, cells engineered to lose their mitochondria (by transfection with Parkin combined with treatment with a protonophore causing mitophagy) were relatively resistant against LTX-315, underscoring the importance of this organelle for LTX-315-mediated cytotoxicity.

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

    27 Oct 2026, 18:20 UTC

    Study results updated

  2. Version 1

    27 Oct 2026, 16:32 UTC

    First added · source update from Europe PMC

Subjects

Terms as the source lists them.

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