ArticleBMC cancer2025
COMP promotes the progression of colorectal cancer by regulating epithelial mesenchymal transition.
Article in BMC cancer, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
3 citing papers in PubMed.
- Cartilage Oligomeric Matrix Protein (COMP) Correlates with Disease Progression, Selected Immune Checkpoint Molecules and SIGLEC9 in Colorectal Cancer.International journal of molecular sciences · 2026Article
- High COMP expression promotes tumor cell proliferation and migration of rectal cancer, contributing to unfavorable prognosis and suppressive immune microenvironment.Discover oncology · 2026Article
- Study on the regulation mechanism of TBX5 gene and Gegen Qinlian decoction on colorectal cancer.Frontiers in oncology · 2025Article
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundEpithelial-mesenchymal transition (EMT) plays a crucial role in the progression and metastasis of colorectal cancer (CRC). This study investigates the molecular mechanisms of EMT and its prognostic biomarkers in CRC.
methodsMulti-omics bioinformatics analyses were conducted using CRC transcriptomic datasets from GEO and TCGA. EMT-related differentially expressed genes (EMT-DEGs) were identified and subjected to pathway enrichment and machine learning-based prognostic modeling. COMP was selected as a hub gene for further validation. Single-cell RNA sequencing (scRNA-seq) data were also analyzed to determine the cell-type-specific expression pattern of COMP and EMT-DEGs. Clinical CRC tissue samples were analyzed via RT-qPCR, Western blot, and histology. Functional assays in HT-29 cells assessed the effects of COMP knockdown on EMT markers, proliferation, apoptosis, invasion, and migration.
resultsEMT was significantly enriched in CRC, with 36 EMT-DEGs identified. These DEGs were enriched in pathways such as ECM-receptor interaction, focal adhesion, and the PI3K-Akt signaling pathway. Among the constructed machine learning models, the random survival forest (RSF) model demonstrated the strongest ability to predict CRC prognosis. This model stratified CRC patients into high-risk and low-risk groups, with poorer prognosis observed in the high-risk group. Cox regression forest plots and Kaplan-Meier survival analysis identified COMP as a top EMT-related prognostic gene enriched in pathways including ECM-receptor interaction and PI3K-Akt signaling. High COMP expression correlated with poor patient prognosis and EMT marker dysregulation in metastatic CRC tissues. In vitro, COMP knockdown significantly reduced mesenchymal markers, restored E-cadherin, and inhibited proliferation and invasion of CRC cells.
conclusionEMT plays a vital role in CRC progression and metastasis, with COMP identified as a key prognostic biomarker and potential therapeutic target. This study provides new insights into the molecular mechanisms and intervention strategies for CRC metastasis.
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