ArticleJournal of translational medicine2024
Spatiotemporal heterogeneity of LMOD1 expression summarizes two modes of cell communication in colorectal cancer.
Article in Journal of translational medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- AKAP12-LMOD1 signaling defines stromal CAF activation and epithelial junction loss in colorectal cancer.Scientific reports · 2026Article
- Article
- Multi-omics analysis identifies DLX4 as a novel biomarker for diagnosis, prognosis, and immune infiltration: from pan-cancer to renal cancer.Discover oncology · 2025Article
- Breaking down physical barriers: strategies to improve lymphocyte infiltration for effective neoantigen-based therapies.Frontiers in immunology · 2025Review
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Authors and funding
10 authors.
Funding
Abstract
Cellular communication (CC) influences tumor development by mediating intercellular junctions between cells. However, the role and underlying mechanisms of CC in malignant transformation remain unknown. Here, we investigated the spatiotemporal heterogeneity of CC molecular expression during malignant transformation. It was found that although both tight junctions (TJs) and gap junctions (GJs) were involved in maintaining the tumor microenvironment (TME), they exhibited opposite characteristics. Mechanistically, for epithelial cells (parenchymal component), the expression of TJ molecules consistently decreased during normal-cancer transformation and is a potential oncogenic factor. For fibroblasts (mesenchymal component), the expression of GJs consistently increased during normal-cancer transformation and is a potential oncogenic factor. In addition, the molecular profiles of TJs and GJs were used to stratify colorectal cancer (CRC) patients, where subtypes characterized by high GJ levels and low TJ levels exhibited enhanced mesenchymal signals. Importantly, we propose that leiomodin 1 (LMOD1) is biphasic, with features of both TJs and GJs. LMOD1 not only promotes the activation of cancer-associated fibroblasts (CAFs) but also inhibits the Epithelial-mesenchymal transition (EMT) program in cancer cells. In conclusion, these findings demonstrate the molecular heterogeneity of CC and provide new insights into further understanding of TME heterogeneity.
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