{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"volume":["15"],"submitter":["Raynaud CM"],"pubmed_abstract":["<h4>Introduction</h4>Colorectal cancer (CRC) is a prevalent malignancy with significant morbidity and mortality worldwide. A deeper understanding of the interaction of cancer cells with other cells in the tumor microenvironment is crucial to devise effective therapeutic strategies. MUC2, a major component of the protective mucus layer in the gastrointestinal tract, has been implicated in CRC progression and immune response regulation.<h4>Method</h4>In this study, we sought to elucidate the relationship between MUC2 expression and immune infiltration within CRC using <i>in vitro</i> models involving two well-established cell lines, HT-29 and LS-174T. By employing CRISPR-mediated MUC2 knockout, we investigated the influence of MUC2 on tumor immune infiltration and its interplay with T cells and NK cells enriched peripheral blood mononuclear cells (PBMCs) in 3D spheroid cultures.<h4>Results</h4>While MUC2 was more abundant in LS-174T cell line compared to HT-29, its knockout resulted in increased immune infiltration solely in the HT-29 cell line, but not in the LS-174T cell line. We revealed that the removal of MUC2 protein was compensated in LS-174T by the expression of other gel-forming mucin proteins (MUC6, MUC5B) commonly expressed in the gastrointestinal epithelium, while this was not observed in HT-29 cell line.<h4>Conclusion</h4>Our study is the first to demonstrate that MUC2 functions as a physical barrier to immune infiltration in colorectal cancer (CRC) <i>in vitro</i>. In HT-29 cells, MUC2 knockout increased immune infiltration, while in LS-174T cells, compensatory expression of other mucins (MUC6, MUC5B) maintained the barrier. These findings reveal the complexity of mucin biology in CRC and suggest that targeting mucin pathways could be a novel therapeutic approach."],"journal":["Frontiers in immunology"],"pagination":["1500374"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11802499"],"repository":["biostudies-literature"],"pubmed_title":["MUC2 expression modulates immune infiltration in colorectal cancer."],"pmcid":["PMC11802499"],"pubmed_authors":["Lo B","Bedognetti D","Al-Shaibi AA","Sanchez A","Hubrack S","Roelands J","Sherif S","Jabeen A","Raynaud CM","Hendrickx W","Ahmed EI"],"additional_accession":[]},"is_claimable":false,"name":"MUC2 expression modulates immune infiltration in colorectal cancer.","description":"<h4>Introduction</h4>Colorectal cancer (CRC) is a prevalent malignancy with significant morbidity and mortality worldwide. A deeper understanding of the interaction of cancer cells with other cells in the tumor microenvironment is crucial to devise effective therapeutic strategies. MUC2, a major component of the protective mucus layer in the gastrointestinal tract, has been implicated in CRC progression and immune response regulation.<h4>Method</h4>In this study, we sought to elucidate the relationship between MUC2 expression and immune infiltration within CRC using <i>in vitro</i> models involving two well-established cell lines, HT-29 and LS-174T. By employing CRISPR-mediated MUC2 knockout, we investigated the influence of MUC2 on tumor immune infiltration and its interplay with T cells and NK cells enriched peripheral blood mononuclear cells (PBMCs) in 3D spheroid cultures.<h4>Results</h4>While MUC2 was more abundant in LS-174T cell line compared to HT-29, its knockout resulted in increased immune infiltration solely in the HT-29 cell line, but not in the LS-174T cell line. We revealed that the removal of MUC2 protein was compensated in LS-174T by the expression of other gel-forming mucin proteins (MUC6, MUC5B) commonly expressed in the gastrointestinal epithelium, while this was not observed in HT-29 cell line.<h4>Conclusion</h4>Our study is the first to demonstrate that MUC2 functions as a physical barrier to immune infiltration in colorectal cancer (CRC) <i>in vitro</i>. In HT-29 cells, MUC2 knockout increased immune infiltration, while in LS-174T cells, compensatory expression of other mucins (MUC6, MUC5B) maintained the barrier. These findings reveal the complexity of mucin biology in CRC and suggest that targeting mucin pathways could be a novel therapeutic approach.","dates":{"release":"2024-01-01T00:00:00Z","publication":"2024","modification":"2026-05-26T17:03:41.564Z","creation":"2025-04-04T13:11:01.77Z"},"accession":"S-EPMC11802499","cross_references":{"pubmed":["39926604"],"doi":["10.3389/fimmu.2024.1500374"]}}