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Study · Animal study (in vivo) · 2016

9 results

The oncolytic peptide LTX-315 triggers immunogenic cell death.

Zhou H, Forveille S, Sauvat A, Yamazaki T, Senovilla L, Ma Y, Liu P, Yang H, Bezu L, Müller K, Zitvogel L, Rekdal Ø, Kepp O, Kroemer G

Cell death & disease10 Mar 2016Cited by 119 (Europe PMC)

PMID26962684 (opens in a new tab)PMCIDPMC4823948 (opens in a new tab)DOI10.1038/cddis.2016.47 (opens in a new tab)PepBankPUB-26962684
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Summary

LTX-315 is a cationic amphilytic peptide that preferentially permeabilizes mitochondrial membranes, thereby causing partially BAX/BAK1-regulated, caspase-independent necrosis. Based on the observation that intratumorally injected LTX-315 stimulates a strong T lymphocyte-mediated anticancer immune response, we investigated whether LTX-315 may elicit the hallmarks of immunogenic cell death (ICD), namely (i) exposure of calreticulin on the plasma membrane surface, (ii) release of ATP into the extracellular space, (iii) exodus of HMGB1 from the nucleus, and (iv) induction of a type-1 interferon response. Using a panel of biosensor cell lines and robotized fluorescence microscopy coupled to automatic image analysis, we observed that LTX-315 induces all known ICD characteristics. This conclusion was validated by several independent methods including immunofluorescence stainings (for calreticulin), bioluminescence assays (for ATP), immunoassays (for HMGB1), and RT-PCRs (for type-1 interferon induction). When injected into established cancers, LTX-315 caused a transiently hemorrhagic focal necrosis that was accompanied by massive release of HMGB1 (from close-to-all cancer cells), as well as caspase-3 activation in a fraction of the cells. LTX-315 was at least as efficient as the positive control, the anthracycline mitoxantrone (MTX), in inducing local inflammation with infiltration by myeloid cells and T lymphocytes. Collectively, these results support the idea that LTX-315 can induce ICD, hence explaining its capacity to mediate immune-dependent therapeutic effects.
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. 01AnimalAnimal study (in vivo)Mechanism

    In established cancers, injected LTX‑315 caused transiently hemorrhagic focal necrosis.

    In plain wordsIn animals with established cancers, LTX‑315 caused temporary bleeding and local tissue death.

    Peptide
    LTX-315
    Outcome
    IncreaseHemorrhagic focal necrosis
    Study

    n: not reported in source

    established cancers
    Outcome group
    Tumor growth · Cancer
    Studied dose
    Dose not stated · intratumoralAs given in this study.

    Source sentences

    Summary
    When injected into established cancers, LTX-315 caused a transiently hemorrhagic focal necrosis that was accompanied by massive release of HMGB1 (from close-to-all cancer cells), as well as caspase-3 activation in a fraction of the cells.
  2. 02AnimalAnimal study (in vivo)Mechanism

    In established cancers, LTX‑315 caused massive HMGB1 release from nearly all cancer cells.

    In plain wordsIn animals with established cancers, LTX‑315 caused large HMGB1 release from nearly all cancer cells.

    Peptide
    LTX-315
    Outcome
    IncreaseHMGB1 release in cancers
    Study

    n: not reported in source

    established cancers
    Outcome group
    Immune response · Cancer
    Studied dose
    Dose not stated · intratumoralAs given in this study.

    Source sentences

    Summary
    When injected into established cancers, LTX-315 caused a transiently hemorrhagic focal necrosis that was accompanied by massive release of HMGB1 (from close-to-all cancer cells), as well as caspase-3 activation in a fraction of the cells.
  3. 03AnimalAnimal study (in vivo)Mechanism

    In established cancers, LTX‑315 activated caspase-3 in a fraction of cells.

    In plain wordsIn animals with established cancers, LTX‑315 activated caspase-3 in some cells.

    Peptide
    LTX-315
    Outcome
    IncreaseCaspase-3 activation
    Study

    n: not reported in source

    established cancers
    Outcome group
    Receptor activity and mechanism · Cancer
    Studied dose
    Dose not stated · intratumoralAs given in this study.

    Source sentences

    Summary
    When injected into established cancers, LTX-315 caused a transiently hemorrhagic focal necrosis that was accompanied by massive release of HMGB1 (from close-to-all cancer cells), as well as caspase-3 activation in a fraction of the cells.
  4. 04AnimalAnimal study (in vivo)Mechanism

    In established cancers, LTX‑315 was at least as efficient as mitoxantrone in inducing local inflammation.

    In plain wordsIn animals with established cancers, LTX‑315 induced local inflammation at least as efficiently as mitoxantrone.

    Peptide
    LTX-315
    Outcome
    Not applicableLocal inflammation
    Study

    n: not reported in source

    established cancers
    Comparator
    mitoxantrone
    Outcome group
    Immune response · Cancer
    Studied dose
    Dose not stated · intratumoralAs given in this study.

    Source sentences

    Summary
    LTX-315 was at least as efficient as the positive control, the anthracycline mitoxantrone (MTX), in inducing local inflammation with infiltration by myeloid cells and T lymphocytes.
  5. 05AnimalAnimal study (in vivo)Mechanism

    In established cancers, LTX‑315 induced myeloid and T-cell infiltration at least as efficiently as mitoxantrone.

    In plain wordsIn animals with established cancers, LTX‑315 induced myeloid and T-cell infiltration at least as efficiently as mitoxantrone.

    Peptide
    LTX-315
    Outcome
    Not applicableMyeloid and T-cell infiltration
    Study

    n: not reported in source

    established cancers
    Comparator
    mitoxantrone
    Outcome group
    Immune response · Cancer
    Studied dose
    Dose not stated · intratumoralAs given in this study.

    Source sentences

    Summary
    LTX-315 was at least as efficient as the positive control, the anthracycline mitoxantrone (MTX), in inducing local inflammation with infiltration by myeloid cells and T lymphocytes.
  6. 06LabIn vitro (cells)Mechanism

    In biosensor cells, LTX‑315 induced calreticulin surface exposure as an immunogenic cell death characteristic.

    In plain wordsIn cells, LTX‑315 induced surface exposure of calreticulin.

    Peptide
    LTX-315
    Outcome
    IncreaseCalreticulin surface exposure
    Study

    n: not reported in source

    biosensor cell lines
    Outcome group
    Immune response · Cancer
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Using a panel of biosensor cell lines and robotized fluorescence microscopy coupled to automatic image analysis, we observed that LTX-315 induces all known ICD characteristics.
    2 context sentences
    Summary · context
    This conclusion was validated by several independent methods including immunofluorescence stainings (for calreticulin), bioluminescence assays (for ATP), immunoassays (for HMGB1), and RT-PCRs (for type-1 interferon induction).
    Summary · context
    namely (i) exposure of calreticulin on the plasma membrane surface, (ii) release of ATP into the extracellular space, (iii) exodus of HMGB1 from the nucleus, and (iv) induction of a type-1 interferon response.
  7. 07LabIn vitro (cells)Mechanism

    In biosensor cells, LTX‑315 induced extracellular ATP release as an immunogenic cell death characteristic.

    In plain wordsIn cells, LTX‑315 induced ATP release outside the cells.

    Peptide
    LTX-315
    Outcome
    IncreaseATP release
    Study

    n: not reported in source

    biosensor cell lines
    Outcome group
    Immune response · Cancer
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Using a panel of biosensor cell lines and robotized fluorescence microscopy coupled to automatic image analysis, we observed that LTX-315 induces all known ICD characteristics.
    2 context sentences
    Summary · context
    This conclusion was validated by several independent methods including immunofluorescence stainings (for calreticulin), bioluminescence assays (for ATP), immunoassays (for HMGB1), and RT-PCRs (for type-1 interferon induction).
    Summary · context
    namely (i) exposure of calreticulin on the plasma membrane surface, (ii) release of ATP into the extracellular space, (iii) exodus of HMGB1 from the nucleus, and (iv) induction of a type-1 interferon response.
  8. 08LabIn vitro (cells)Mechanism

    In biosensor cells, LTX‑315 induced HMGB1 nuclear exodus as an immunogenic cell death characteristic.

    In plain wordsIn cells, LTX‑315 caused HMGB1 to leave the nucleus.

    Peptide
    LTX-315
    Outcome
    IncreaseHMGB1 nuclear exodus
    Study

    n: not reported in source

    biosensor cell lines
    Outcome group
    Immune response · Cancer
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Using a panel of biosensor cell lines and robotized fluorescence microscopy coupled to automatic image analysis, we observed that LTX-315 induces all known ICD characteristics.
    2 context sentences
    Summary · context
    This conclusion was validated by several independent methods including immunofluorescence stainings (for calreticulin), bioluminescence assays (for ATP), immunoassays (for HMGB1), and RT-PCRs (for type-1 interferon induction).
    Summary · context
    namely (i) exposure of calreticulin on the plasma membrane surface, (ii) release of ATP into the extracellular space, (iii) exodus of HMGB1 from the nucleus, and (iv) induction of a type-1 interferon response.
  9. 09LabIn vitro (cells)Mechanism

    In biosensor cells, LTX‑315 induced a type-1 interferon response.

    In plain wordsIn cells, LTX‑315 induced a type-1 interferon response.

    Peptide
    LTX-315
    Outcome
    IncreaseType-1 interferon response
    Study

    n: not reported in source

    biosensor cell lines
    Outcome group
    Immune response · Cancer
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Using a panel of biosensor cell lines and robotized fluorescence microscopy coupled to automatic image analysis, we observed that LTX-315 induces all known ICD characteristics.
    1 context sentence
    Summary · context
    This conclusion was validated by several independent methods including immunofluorescence stainings (for calreticulin), bioluminescence assays (for ATP), immunoassays (for HMGB1), and RT-PCRs (for type-1 interferon induction).

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

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