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Study · Animal study (in vivo) · mouse · 2022

3 results

Oncolytic peptide LTX-315 induces anti-pancreatic cancer immunity by targeting the ATP11B-PD-L1 axis.

Tang T, Huang X, Zhang G, Lu M, Hong Z, Wang M, Huang J, Zhi X, Liang T

Journal for immunotherapy of cancer1 Mar 2022Cited by 22 (Europe PMC)

PMID35288467 (opens in a new tab)PMCIDPMC8921947 (opens in a new tab)DOI10.1136/jitc-2021-004129 (opens in a new tab)PepBankPUB-35288467
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Summary

BackgroundLTX-315 is an oncolytic peptide deriving from bovine lactoferrin, with the ability to induce cancer immunogenic cell death. However, the mechanism used by LTX-315 to trigger the antitumor immune response is still poorly understood. The expression of programmed cell death ligand 1 (PD-L1) largely determines the efficacy and effectiveness of cancer immunotherapies targeting this specific immune checkpoint. This study aimed to demonstrate the potential effect and mechanism of LTX-315 in PD-L1 inhibition-induced anti-pancreatic cancer immunity.MethodsBoth immunodeficient and immunocompetent mouse models were used to evaluate the therapeutic efficacy of monotherapy and combination therapy. Flow cytometry and immunohistochemistry were used to assess the immune microenvironment. Multiomic analysis was used to identify the potential target and down-streaming signaling pathway. Both in-house tissue microarray and open accessed The Cancer Genome Atlas data sets were used to evaluate the clinical relevance in pancreatic cancer prognosis.ResultsLTX-315 treatment inhibited PD-L1 expression and enhanced lymphocyte infiltration in pancreatic tumors. ATP11B was identified as a potential target of LTX-315 and a critical regulator in maintaining PD-L1 expression in pancreatic cancer cells. As regards the mechanism, ATP11B interacted with PD-L1 in a CKLF-like MARVEL transmembrane domain containing 6 (CMTM6)-dependent manner. The depletion of ATP11B promoted CMTM6-mediated lysosomal degradation of PD-L1, thus reactivating the immune microenvironment and inducing an antitumor immune response. The significant correlation among ATP11B, CMTM6, and PD-L1 was confirmed in clinical samples of pancreatic cancer.ConclusionsLTX-315 was first identified as a peptide drug inducing PD-L1 downregulation via ATP11B. Therefore, LTX-315, or the development of ATP11B-targeting drugs, might improve the efficacy of cancer immunotherapy.
CC BYText from Europe PMC. Highlighted sentences are the source of results.

Results from this study3

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

  1. 01AnimalAnimal study (in vivo)Mechanism

    In mouse pancreatic tumors, LTX‑315 inhibited PD-L1 expression.

    In plain wordsIn mice, LTX‑315 reduced PD-L1 expression in pancreatic tumors.

    Peptide
    LTX-315
    Outcome
    DecreasePD-L1 expression
    Study

    mousen: not reported in source

    Pancreatic tumors
    Outcome group
    Receptor activity and mechanism · Cancer
    Studied dose
    Dose not stated

    Source sentences

    Summary
    LTX-315 treatment inhibited PD-L1 expression and enhanced lymphocyte infiltration in pancreatic tumors.
    1 context sentence
    Summary · context
    Both immunodeficient and immunocompetent mouse models were used to evaluate the therapeutic efficacy of monotherapy and combination therapy.
  2. 02AnimalAnimal study (in vivo)Mechanism

    In mouse pancreatic tumors, LTX‑315 enhanced lymphocyte infiltration.

    In plain wordsIn mice, LTX‑315 increased lymphocyte entry into pancreatic tumors.

    Peptide
    LTX-315
    Outcome
    IncreaseLymphocyte infiltration
    Study

    mousen: not reported in source

    Pancreatic tumors
    Outcome group
    Immune response · Cancer
    Studied dose
    Dose not stated

    Source sentences

    Summary
    LTX-315 treatment inhibited PD-L1 expression and enhanced lymphocyte infiltration in pancreatic tumors.
    1 context sentence
    Summary · context
    Both immunodeficient and immunocompetent mouse models were used to evaluate the therapeutic efficacy of monotherapy and combination therapy.
  3. 03LabIn vitro (cells)Mechanism

    In pancreatic cancer cells, ATP11B was identified as a potential LTX‑315 target that maintains PD-L1 expression.

    In plain wordsIn cells, ATP11B was identified as a possible LTX‑315 target involved in PD-L1 expression.

    Peptide
    LTX-315
    Outcome
    Not applicableATP11B target identification
    Study

    n: not reported in source

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

    Source sentences

    Summary
    ATP11B was identified as a potential target of LTX-315 and a critical regulator in maintaining PD-L1 expression in pancreatic cancer cells.

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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