{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,30]],"date-time":"2026-03-30T06:54:25Z","timestamp":1774853665023,"version":"3.50.1"},"reference-count":65,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2026,3,30]],"date-time":"2026-03-30T00:00:00Z","timestamp":1774828800000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Immunol."],"abstract":"<jats:sec>\n                    <jats:title>Introduction<\/jats:title>\n                    <jats:p>\n                      Colorectal cancer (CRC) remains a leading cause of cancer-related mortality. Plantaricin BM-1, a class IIa bacteriocin from Lactobacillus plantarum, exhibits anticancer potential, but its\n                      <jats:italic>in vivo<\/jats:italic>\n                      efficacy against CRC is unclear.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>Using an AOM\/DSS-induced CRC mouse model, we administered Plantaricin BM-1 orally and evaluated therapeutic effects via phenotypic, pathological, and inflammatory assessments. scRNA-seq elucidated molecular mechanisms, validated by RT-qPCR, IHC, flow cytometry, and Western blot.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Discussion<\/jats:title>\n                    <jats:p>\n                      ResultsResults demonstrated that Plantaricin BM-1 significantly suppressed tumorigenesis, colon shortening, serum TNF-\u03b1 levels, and pathological damage. scRNA-seq revealed a 17.38% increase in tumor-infiltrating T cells and a 9.29% expansion of cytotoxic CD8\u207a T cells. Key cytotoxic genes (Gzma, Gzmb, Fasl) were upregulated in CD8\u207a T cells, while the ERK\/AP1 pathway was suppressed. Consistently, Plantaricin BM-1 downregulated ERK, AP1, and pro-apoptotic Bim\n                      <jats:italic>in vivo<\/jats:italic>\n                      and\n                      <jats:italic>in vitro<\/jats:italic>\n                      . Crucially, it inhibited CD8\u207a T cell apoptosis via the ERK\/AP1 pathway.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Discussion<\/jats:title>\n                    <jats:p>These findings provide mechanistic insights for developing Plantaricin BM-1 as an anti-CRC agent.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.3389\/fimmu.2026.1792962","type":"journal-article","created":{"date-parts":[[2026,3,30]],"date-time":"2026-03-30T05:27:21Z","timestamp":1774848441000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":0,"title":["Plantaricin BM-1 enhances anti-colorectal cancer effects by inhibiting CD8+ cytotoxic T cell apoptosis via the ERK\/AP1\/Bim signaling pathway"],"prefix":"10.3389","volume":"17","author":[{"given":"Xuan","family":"Zheng","sequence":"first","affiliation":[{"name":"Beijing Laboratory of Food Quality and Safety, Beijing 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