PMID- 1555895
OWN - NLM
STAT- MEDLINE
DCOM- 19920505
LR  - 20190708
IS  - 0020-7136 (Print)
IS  - 0020-7136 (Linking)
VI  - 50
IP  - 6
DP  - 1992 Apr 1
TI  - Regulation of human colon-carcinoma cell adhesion to extracellular matrix by 
      transforming growth factor beta 1.
PG  - 968-73
AB  - The regulatory effect of transforming growth factor beta 1 (TGF-beta 1) on the 
      adhesion of human colon-carcinoma cells to the extracellular matrix (ECM) was 
      investigated. ECMs used in this study included tissue-culture wells coated with 
      fibronectin, laminin, collagen and BSA, as well as plastic wells. Three 
      phenotypically different human colon-carcinoma cell lines (Moser, HCT116, and 
      KM12SM) were used. The Moser cell line is moderately differentiated and, in terms 
      of the diversity of responses elicited by TGF-beta 1, is the human 
      colon-carcinoma cell line most responsive to TGF-beta 1 as reported to date. By 
      comparison, the undifferentiated HCT116 and the highly metastatic KM12SM cells 
      are unresponsive to this growth factor. We showed that TGF-beta 1 regulated the 
      adhesion responses of all 3 cell lines. However, the response profiles as well as 
      the endogenous adhesive properties of each cell line were quite different from 
      those of the others. Endogenous Arg-Gly-Asp(RGD)-related receptors were present 
      on the HCT116 but not on the other cells. The observed regulatory effect of 
      TGF-beta 1 was contingent on the cell line, the type of ECM, and the 
      growth-factor treatment protocol used. When cells were treated with TGF-beta 1 
      for 16 hr prior to exposure to ECM in a 4-hr adhesion assay, a significant 
      increase in adhesion to fibronectin and collagen was observed for the Moser 
      cells. For the identical experimental protocol, the KM12SM cells responded by 
      increasing adhesion to fibronectin, while the HCT116 cells responded by 
      decreasing adhesion to collagen. Kinetic analyses of TGF-beta 1 treatment showed 
      that increased adhesion response to laminin was induced in the Moser cells after 
      2 hr of growth-factor treatment. This response declined rapidly upon further 
      exposure of the cells to TGF-beta 1. Simultaneous exposure of cells to both 
      TGF-beta 1 and ECM negated the adhesion responses described above. The 
      up-modulation of adhesion to fibronectin, laminin and collagen by TGF-beta 1 was 
      mediated through RGD-related integrin receptors. RGD-containing peptides 
      effectively blocked the enhanced adhesion responses induced by TGF-beta 1.
FAU - Chakrabarty, S
AU  - Chakrabarty S
AD  - Division of Laboratory Medicine, University of Texas, M.D. Anderson Cancer 
      Center, Houston 77030.
LA  - eng
GR  - CA 47775/CA/NCI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - Int J Cancer
JT  - International journal of cancer
JID - 0042124
RN  - 0 (Oligopeptides)
RN  - 0 (Receptors, Immunologic)
RN  - 0 (Receptors, Peptide)
RN  - 0 (Transforming Growth Factor beta)
RN  - 0 (arginyl-glycyl-aspartic acid directed cell adhesion receptor)
RN  - 78VO7F77PN (arginyl-glycyl-aspartic acid)
SB  - IM
MH  - Amino Acid Sequence
MH  - Cell Adhesion/*drug effects
MH  - Cell Line
MH  - Colonic Neoplasms/*physiopathology
MH  - Extracellular Matrix/*physiology
MH  - Humans
MH  - Kinetics
MH  - Oligopeptides/pharmacology
MH  - Receptors, Immunologic/drug effects/physiology
MH  - *Receptors, Peptide
MH  - Time Factors
MH  - Transforming Growth Factor beta/*pharmacology
MH  - Tumor Cells, Cultured
EDAT- 1992/04/01 00:00
MHDA- 1992/04/01 00:01
CRDT- 1992/04/01 00:00
PHST- 1992/04/01 00:00 [pubmed]
PHST- 1992/04/01 00:01 [medline]
PHST- 1992/04/01 00:00 [entrez]
AID - 10.1002/ijc.2910500624 [doi]
PST - ppublish
SO  - Int J Cancer. 1992 Apr 1;50(6):968-73. doi: 10.1002/ijc.2910500624.