ArticleHeliyon2024
The COL7A1/PI3K/AKT axis regulates the progression of cholangiocarcinoma.
Article in Heliyon, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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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
5 citing papers in PubMed.
- Identification of Paraptosis-Related Renal Cell Carcinoma Subtypes, Construction of a Prognostic Signature, and Determination of Tumor Microenvironment Landscape Using Bioinformatic Analysis and Experimental Verification.Current issues in molecular biology · 2026Article
- Depression of tryptophan may contribute to adverse effects of naproxen.Nature communications · 2026Article
- Identification of cancer-associated fibroblast signature genes for potential biomarkers in cholangiocarcinoma: a Mendelian randomization study.Discover oncology · 2025Article
- Application and mechanism of anticancer peptides in organoid models of intrahepatic cholangiocarcinoma.Scientific reports · 2025Article
- Integrative Machine Learning and Bioinformatics Approach for Identifying Key Biomarkers in Gallbladder Cancer Diagnosis and Progression.IET systems biologyArticle
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Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: The role and molecular mechanisms of collagen type VII (COL7A1) in cholangiocarcinoma (CCA) remain unknown. Methods: We analyzed the expression of COL7A1 in CCA and its relationship with patient prognosis using bioinformatic techniques. Expression levels of COL7A1 in CCA cells and tissues were detected using reverse transcription-quantitative PCR, western blotting, and immunohistochemistry. The effects of COL7A1 expression on the proliferation, migration, and invasion of CCA cells were assessed using CCK-8, colony formation, and Transwell assays. Bioinformatics and luciferase reporter gene assays were performed to examine the binding of KLF4 to COL7A1, and cytological experiments further verified the role of KLF4 in regulating the CCA phenotype through COL7A1. Xenograft mouse models were established to investigate the effects of COL7A1 on CCA tumor growth Results: CCA tissues exhibited higher COL7A1 expression than normal bile duct tissues. There was no significant correlation between high or low COL7A1 expression and the survival time of patients with CCA. COL7A1 knockdown inhibited CCA cell proliferation, migration, and invasion. Furthermore, COL7A1 knockdown suppressed the activation of the PI3K/AKT signaling pathway. KLF4 can bind to COL7A1 and regulate COL7A1 expression, which in turn regulates the PI3K/AKT signaling pathway and impacts the proliferation and metastasis of CCA cells. Conclusion: Our findings suggest that KLF4 regulates CCA cell proliferation, migration, and invasion via the COL7A1/PI3K/AKT axis.
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