alexa Type I collagen inhibits differentiation and promotes a stem cell-like phenotype in human colorectal carcinoma cells.


Biochemistry & Physiology: Open Access

Author(s): Kirkland SC

Abstract Share this page

Abstract BACKGROUND: Human colorectal cancer is caused by mutations and is thought to be maintained by a population of cancer stem cells. Further phenotypic changes occurring at the invasive edge suggest that colon cancer cells are also regulated by their microenvironment. Type I collagen, a promoter of the malignant phenotype in pancreatic carcinoma cells, is highly expressed at the invasive front of human colorectal cancer. METHODS: This study investigates the role of type I collagen in specifying the colorectal cancer cell phenotype. The effect of type I collagen on morphology, localisation of cell-cell adhesion proteins, differentiation and stem cell-like characteristics was examined in a panel of human colorectal carcinoma cell lines. RESULTS: Human colorectal carcinoma cells grown on type I collagen in serum-free medium show an epithelial-mesenchymal-like transition (EMT-like), assuming a more flattened less cohesive morphology. Type I collagen downregulates E-cadherin and beta-catenin at cell-cell junctions. Furthermore, type I collagen inhibits differentiation, increases clonogenicity and promotes expression of stem cell markers CD133 and Bmi1. Type I collagen effects were partially abrogated by a function-blocking antibody to alpha2 integrin. CONCLUSION: Together, these results indicate that type I collagen promotes expression of a stem cell-like phenotype in human colorectal cancer cells likely through alpha2beta1 integrin.
This article was published in Br J Cancer and referenced in Biochemistry & Physiology: Open Access

Relevant Expert PPTs

Relevant Speaker PPTs

Recommended Conferences

  •  2nd International Conference on Biochemistry
    Sep 21-22, 2017, Macau, Hong Kong

Relevant Topics

Peer Reviewed Journals
Make the best use of Scientific Research and information from our 700 + peer reviewed, Open Access Journals
International Conferences 2017-18
Meet Inspiring Speakers and Experts at our 3000+ Global Annual Meetings

Contact Us

© 2008-2017 OMICS International - Open Access Publisher. Best viewed in Mozilla Firefox | Google Chrome | Above IE 7.0 version