ArticleWorld journal of gastrointestinal oncology2024
Complement factor I knockdown inhibits colon cancer development by affecting Wnt/β-catenin/c-Myc signaling pathway and glycolysis.
Article in World journal of gastrointestinal oncology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Tumour cell-intrinsic complement C1r and C1s regulate cancer cell fitness and shape the immune microenvironment in triple-negative breast cancer.Cellular and molecular life sciences : CMLS · 2026Article
- NR4A1 Regulates Glycolysis in M1 Macrophages via the Wnt/β-Catenin Pathway to Affect Sepsis-Induced Myocardial Injury.Journal of inflammation research · 2026Article
- Identification of EFNA3 as candidate prognosis marker and potential therapeutic target for adrenocortical carcinoma.Oncology letters · 2025Article
- Comparative Gene Expression Analysis of Malignant Mesothelioma and Lung Adenocarcinomas Induced by Multi-Walled Carbon Nanotube-7 and Double-Walled Carbon Nanotubes in Rats: Distinct Molecular Signatures and Canonical Pathways.Nanomaterials (Basel, Switzerland) · 2025Article
- Gut complement system: a new frontier in microbiota-host communication and intestinal homeostasis.The Journal of clinical investigation · 2025Review
- Wnt signaling in cancer: from biomarkers to targeted therapies and clinical translation.Molecular cancer · 2025Review
- New insights into the role of complement system in colorectal cancer (Review).Molecular medicine reports · 2025Review
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4 authors.
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No grant is acknowledged in the PubMed record.
Abstract
backgroundColon cancer (CC) occurrence and progression are considerably influenced by the tumor microenvironment. However, the exact underlying regulatory mechanisms remain unclear.
aimTo investigate immune infiltration-related differentially expressed genes (DEGs) in CC and specifically explored the role and potential molecular mechanisms of complement factor I (CFI).
methodsImmune infiltration-associated DEGs were screened for CC using bioinformatics. Quantitative reverse transcription polymerase chain reaction was used to examine hub DEGs expression in the CC cell lines. Stable CFI-knockdown HT29 and HCT116 cell lines were constructed, and the diverse roles of CFI
resultsSix key immune infiltration-related DEGs were screened, among which the expression of CFI, complement factor B, lymphoid enhancer binding factor 1, and SRY-related high-mobility-group box 4 was upregulated, whereas that of fatty acid-binding protein 1, and bone morphogenic protein-2 was downregulated. Furthermore, CFI could be used as a diagnostic biomarker for CC. Functionally, CFI silencing inhibited CC cell proliferation, migration, invasion, and tumor growth. Mechanistically, CFI knockdown downregulated the expression of key glycolysis-related proteins (glucose transporter type 1, hexokinase 2, lactate dehydrogenase A, and pyruvate kinase M2) and the Wnt pathway-related proteins (β-catenin and c-Myc). Further investigation indicated that CFI knockdown inhibited glycolysis in CC by blocking the Wnt/β-catenin/c-Myc pathway.
conclusionThe findings of the present study demonstrate that CFI plays a crucial role in CC development by influencing glycolysis and the Wnt/β-catenin/c-Myc pathway, indicating that it could serve as a promising target for therapeutic intervention in CC.
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