ArticleOncotarget2018
Collagen XVII/laminin-5 activates epithelial-to-mesenchymal transition and is associated with poor prognosis in lung cancer.
Article in Oncotarget, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 53 citations in OpenAlex.
- Adherens junction protein expression is associated with poor response to neoadjuvant FLOT chemotherapy and pro-inflammatory tumor microenvironment in esophageal adenocarcinoma.International journal of cancer · 2026Article
- Morphological abnormalities in the ureter of type XVII collagen-deficient mice.Scientific reports · 2026Article
- Photocrosslinkable lung dECM hydrogels promote stiffness-dependent lung cancer growth and chemoresistance.Materials today. Bio · 2026Article
- Senescent epithelial cells remodel the tumor microenvironment and drive early LUAD progression: a multiomics risk model and single-cell analysis.Cellular and molecular life sciences : CMLS · 2026Article
- The role of ADAM8 in intrahepatic cholangiocarcinoma.Discover oncology · 2025Review
- Tissue mechanics in tumor heterogeneity and aggression.Trends in cancer · 2025Review
- Collagen XVII Promotes Pancreatic Ductal Adenocarcinoma Tumor Growth through Regulation of PIK3R5.Cancer research communications · 2025Article
- The role of LAMA5 in breast cancer progression and its potential in immunotherapy.Discover oncology · 2025Article
- Decoding chromosomal instability insights in CRC by integrating omics and patient-derived organoids.Journal of experimental & clinical cancer research : CR · 2025Article
- The role of laminins in cancer pathobiology: a comprehensive review.Journal of translational medicine · 2025Review
- Harnessing the tumor microenvironment: targeted cancer therapies through modulation of epithelial-mesenchymal transition.Journal of hematology & oncology · 2025Review
- Basal-epithelial subpopulations underlie and predict chemotherapy resistance in triple-negative breast cancer.EMBO molecular medicine · 2024Article
- Tumor Microenvironment: A Niche for Cancer Stem Cell Immunotherapy.Stem cell reviews and reports · 2024Review
- Unveiling Collagen's Role in Breast Cancer: Insights into Expression Patterns, Functions and Clinical Implications.International journal of general medicine · 2024Review
- G protein-coupled estrogen receptor 1 and collagen XVII endodomain expression in human cutaneous melanomas: can they serve as prognostic factors?Pathology oncology research : POR · 2024Article
- The Nexus of Inflammation-Induced Epithelial-Mesenchymal Transition and Lung Cancer Progression: A Roadmap to Pentacyclic Triterpenoid-Based Therapies.International journal of molecular sciences · 2023Review
- MAPKs in the early steps of senescence implemEMTation.Frontiers in cell and developmental biology · 2023Article
- Function and prognostic value of basement membrane -related genes in lung adenocarcinoma.Frontiers in pharmacology · 2023Article
- Alcohol promotes epithelial mesenchymal transformation-mediated premetastatic niche formation of colorectal cancer by activating interaction between laminin-γ2 and integrin-β1.World journal of gastroenterology · 2022Article
- Decreased Expression of LAMB3 Is Associated with Esophageal Cancer Stem Cell Formation.Advanced pharmaceutical bulletin · 2022Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Epithelial-to-mesenchymal transition (EMT) is associated with tumor metastasis and tumorigenesis in lung cancer stem-like cells (CSCs). However, the exact mechanism underlying this is not clear. We used microarray analysis to identify candidate genes responsible for EMT in spheroid and monolayer cultures of lung cancer cells. We found increased expression of a variety of adhesion molecules in CSCs. One of these molecules, Collagen XVII (Col XVII), was demonstrated to be required for maintenance of EMT phenotypes and metastasis ability in lung CSCs. We showed that Col XVII stabilized laminin-5 to activate the FAK/AKT/GSK3β pathway, thereby suppressing Snail ubiquitination-degradation. The function of Col XVII was mainly dependent on shedding by ADAM9 and ADAM10. Patients who underwent surgical resection for lung cancer, and displayed overexpression of both Col XVII and laminin-5, had the worst prognosis of all expression types. Moreover, blockage of the Col XVII/laminin-5 pathway reduced the EMT phenotypes of lung CSCs
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.