ArticleJournal of experimental & clinical cancer research : CR2023
MYL9 expressed in cancer-associated fibroblasts regulate the immune microenvironment of colorectal cancer and promotes tumor progression in an autocrine manner.
Article in Journal of experimental & clinical cancer research : CR, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 45 citations in OpenAlex.
- Microenvironment-aware transcriptome reconstruction in spatial transcriptomics.Nature communications · 2026Article
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- IQGAP Family Proteins in Colorectal Cancer: Molecular Mechanisms and Prognostic Implications.Diagnostics (Basel, Switzerland) · 2026Review
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- Cytokines and cancer-associated fibroblasts.Journal of hematology & oncology · 2026Review
- Integrative GWAS and RNA-seq identify MYL9 as a key regulator of pullorum disease resistance in chickens.Poultry science · 2026Article
- Integrated bulk RNA-seq and scRNA-seq identification of a novel "PET-Translational cancer research · 2026Article
- Key molecular mechanisms and regulatory networks in colorectal cancer liver metastasis.Biological procedures online · 2026Review
- Crosstalk between SPP1+ macrophages and ITGA5+ fibroblasts promotes hepatocellular carcinoma metastasis.Hepatology communications · 2026Article
- Integrative analyses of metastatic cancer transcriptome reveal clinically distinct cellular States and ecosystems.Scientific reports · 2026Article
- Innate immune signaling-driven myeloid remodeling in cancer: inflammatory amplification, immune suppression, and therapeutic targeting.Frontiers in immunology · 2026Review
- Integrated single-cell and spatial transcriptomic analyses identify TRIP6 as a prognostic and EMT-associated biomarker in colorectal cancer.Frontiers in cell and developmental biology · 2026Article
- Spatial Transcriptomics Reveals Distinct Architectures but Shared Vulnerabilities in Primary and Metastatic Liver Tumors.Cancers · 2025Article
- Effect of Reoxygenation on Radioresistance of Chronically Hypoxic A549 Non-Small Cell Lung Cancer (NSCLC) Cells Following X-Ray and Carbon Ion Exposure.International journal of molecular sciences · 2025Article
- PDPN+ cancer-associated fibroblasts correlate with the neoadjuvant immunotherapy response in gastric cancer.APL bioengineering · 2025Article
- Tumor microenvironment in osteosarcoma: From cellular mechanism to clinical therapy.Genes & diseases · 2025Review
- BRD8 inhibits colorectal cancer progression through TGF-β1-mediated tumor-associated macrophage recruitment.Discover oncology · 2025Article
- Epithelial-mesenchymal transition in colorectal cancer metastasis and progression: molecular mechanisms and therapeutic strategies.Cell death discovery · 2025Review
- DNMBP-AS1/hsa-miR-30a-5p/PGC1α axis suppresses tumor progression of colorectal cancer by inhibiting PKM2-mediated Warburg effect and enhance anti-PD-1 therapy efficacy.Cell death discovery · 2025Article
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Authors and funding
10 authors at 2 institutions in 1 country.
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Abstract
backgroundThe tumor microenvironment (TME) is an important factor that regulates the progression of colorectal cancer (CRC). Cancer-associated fibroblasts (CAFs) are the main mesenchymal cells in the TME and play a vital role in tumor progression; however, the specific underlying mechanisms require further study.
methodsMultiple single-cell and transcriptome data were analyzed and validated. Primary CAFs isolation, CCK8 assay, co-culture assay, western blotting, multiple immunofluorescence, qRT-PCR, ELISA, immunoprecipitation, ChIP, double luciferase, and animal experiments were used to explore the potential mechanism of MYL9 regulation in CRC.
resultsOur findings revealed that MYL9 was predominantly localized and expressed in CAFs rather than in CRC cells, and bioinformatics analysis revealed that high MYL9 expression was strongly associated with poor overall and disease-free survival in various tumors. In addition, high MYL9 expression is closely associated with M2 macrophage infiltration, which can lead to an immunosuppressive microenvironment in CRC, making it insensitive to immunotherapy. Mechanically, MYL9 can regulate the secretion of CAFs on CCL2 and TGF-β1, thus affecting the immune microenvironment and progression of CRC. In addition, MYL9 bounded with IQGAP1 to regulate CCL2 and TGF-β1 secretion through the ERK 1/2 pathway, and CCL2 and TGF-β1 synergistically promoted CRC cells progression through the PI3K-AKT pathway. Furthermore, MYL9 promotes epithelial-mesenchymal transition (EMT) in CRC. During the upstream regulation of MYL9 in CAFs, we found that the EMT transcription factor ZEB1 could bind to the MYL9 promoter in CAFs, enhancing the activity and function of MYL9. Therefore, MYL9 is predominantly expressed in CAFs and can indirectly influence tumor biology and EMT by affecting CAFs protein expression in CRC.
conclusionsMYL9 regulates the secretion of cytokines and chemokines in CAFs, which can affect the immune microenvironment of CRC and promote CRC progression. The relationship between MYL9 expression and CRC clinical staging and immunotherapy is closer in CAFs than in tumor cells; therefore, studies using CAFs as a model deserve more attention when exploring tumor molecular targets in clinical research.
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