ArticleJournal for immunotherapy of cancer2022
Oncolytic peptide LTX-315 induces anti-pancreatic cancer immunity by targeting the ATP11B-PD-L1 axis.
Article in Journal for immunotherapy of cancer, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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17 citing papers in PubMed, 22 citations in OpenAlex.
- Self-assembled manganese-based nanoplatforms synergizing immunogenic cell death and STING activation for triple-negative breast cancer.Materials today. Bio · 2026Article
- Harnessing Membrane-Active Peptides for Selective Cancer Targeting: Phosphatidylserine Recognition by Tilapia Piscidin 4.JACS Au · 2026Article
- Immunobiological mechanisms of action of oncolytic peptides.Journal for immunotherapy of cancer · 2026Review
- Oncolytic peptide LTX-315 targets PD-L1 to improve antitumor immune response of nanosecond pulse electric field in liver cancer.Journal for immunotherapy of cancer · 2026Article
- Next-Generation Anticancer Peptides: Engineering, Nanotheranostics and Clinical Translation.Nanotheranostics · 2026Review
- ATP11B triggers the infiltration of T cells into GBM and intensifies anti-GBM immunity by upregulating and externalizing S1PR1.Journal of translational medicine · 2025Article
- Substrates, regulation, cellular functions, and disease associations of P4-ATPases.Communications biology · 2025Review
- Insights into therapeutic peptides in the cancer-immunity cycle: Update and challenges.Acta pharmaceutica Sinica. B · 2024Review
- Depleting profibrotic macrophages using bioactivated in vivo assembly peptides ameliorates kidney fibrosis.Cellular & molecular immunology · 2024Article
- Flipping the script: Advances in understanding how and why P4-ATPases flip lipid across membranes.Biochimica et biophysica acta. Molecular cell research · 2024Review
- Review
- From oncolytic peptides to oncolytic polymers: A new paradigm for oncotherapy.Bioactive materials · 2024Review
- CMTM6 as a potential therapy target is associated with immunological tumor microenvironment and can promote migration and invasion in pancreatic adenocarcinoma.Functional & integrative genomics · 2023Article
- Type IV P-Type ATPases: Recent Updates in Cancer Development, Progression, and Treatment.Cancers · 2023Review
- Multifaceted Effects of Kinase Inhibitors on Pancreatic Cancer Cells Reveals Pivotal Entities with Therapeutic Implications.Biomedicines · 2023Article
- Transcriptional control of pancreatic cancer immunosuppression by metabolic enzyme CD73 in a tumor-autonomous and -autocrine manner.Nature communications · 2023Article
- Oncolytic immunotherapy: multiple mechanisms of oncolytic peptides to confer anticancer immunity.Journal for immunotherapy of cancer · 2022Article
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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.
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