PMID- 19568234
OWN - NLM
STAT- MEDLINE
DA  - 20090715 
DCOM- 20090720
LR  - 20090922 
IS  - 1532-1827 (Electronic)
VI  - 101
IP  - 2
DP  - 2009 Jul 21
TI  - Type I collagen inhibits differentiation and promotes a stem cell-like phenotype
      in human colorectal carcinoma cells.
PG  - 320-6
AB  - 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.
AD  - Department of Histopathology, Imperial College London, DuCane Road, London W12 ONN, UK. s.kirkland@imperial.ac.uk
FAU - Kirkland S C
AU  - Kirkland SC
LA  - eng
GR  - 060688 / Wellcome Trust / United Kingdom
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20090630
PL  - England
TA  - Br J Cancer
JT  - British journal of cancer
JID - 0370635
RN  - 0(AC133 antigen)
RN  - 0(Antigens, CD)
RN  - 0(Collagen Type I)
RN  - 0(Glycoproteins)
RN  - 0(Integrin alpha2beta1)
SB  - IM
MH  - Antigens, CD/metabolism
MH  - Caco-2 Cells
MH  - Cell Adhesion/physiology
MH  - Cell Communication/physiology
MH  - Cell Differentiation/*physiology
MH  - Cell Line, Tumor
MH  - Collagen Type I/*metabolism
MH  - Colorectal Neoplasms/metabolism/*pathology
MH  - Epithelial Cells/metabolism/pathology
MH  - Glycoproteins/metabolism
MH  - Humans
MH  - Immunohistochemistry
MH  - Integrin alpha2beta1/metabolism
MH  - Mesoderm/metabolism/pathology
MH  - Neoplastic Stem Cells/metabolism/*pathology
MH  - Nuclear Proteins/metabolism
MH  - Peptides/metabolism
MH  - Proto-Oncogene Proteins/metabolism
MH  - Repressor Proteins/metabolism
PMC - PMC2720218 [Available on 07/21/10]
OID - NLM:PMC2720218 [Available on 07/21/10]
EDAT- 2009/07/02 09:00
MHDA- 2009/07/21 09:00
CRDT- 2009/07/02 09:00
PHST- 2009/06/30 00:00[aheadofprint]
PHST- 2010/07/21 00:00[pmc-release]
AID - 6605143[pii]
AID - 10.1038/sj.bjc.6605143[doi]
PST - ppublish
SO  - Br J Cancer. 2009 Jul21 ; 101(2):320-6 Epub 2009 06 30.