CG&D
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Cancer Research Clinical Cancer Research
Cancer Epidemiology Biomarkers & Prevention Molecular Cancer Therapeutics
Molecular Cancer Research Cell Growth & Differentiation

This Article
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Hafez, M. M.
Right arrow Articles by Friedman, E.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Hafez, M. M.
Right arrow Articles by Friedman, E.

Cell Growth & Differentiation, Vol 1, Issue 12 617-626, Copyright © 1990 by American Association of Cancer Research


ARTICLES

Transforming growth factor beta 1 acts as an autocrine-negative growth regulator in colon enterocytic differentiation but not in goblet cell maturation

MM Hafez, D Infante, S Winawer and E Friedman
Department of Medicine, Memorial Sloan-kettering Cancer Center, New York, New York 10021.

Previous studies from this laboratory (Schroy, P., Rifkin, J., Coffey, R.J., Winawer, S., and Friedman, E. (Cancer Res., 50: 261-265, 1990; Schroy, P.C., Winawer, S., and Friedman, E. Cancer Lett., 48: 53-58, 1989) found that a 7-day treatment of the human colon carcinoma cell line HT29 with the differentiation agent hexamethylene bisacetamide (HMBA) induces both a 4-5-fold increase in transforming growth factor beta 1 (TGF beta 1) mRNA levels and reduced tumorigenicity in vivo. A series of 15 cloned lines with different commitments to differentiation has been isolated from 20-day HMBA-treated HT29 cells, maintained without HMBA, and utilized to study the role of TGF beta 1 in colon carcinoma differentiation. Two such lines, HD6 and HD8, differentiate to 97 and 76% mucus-secreting goblet cells, respectively, in columnar monolayers in postconfluent culture. Both HD6 and HD8 cells exhibit low TGF beta 1 mRNA levels, little different from the undifferentiated HT29 parental line, and exhibit no growth modulation in response to exogenous TGF beta 1. In contrast, two other lines, HD3 and HD4, differentiate to fluid-transporting enterocytic cells with functional brush borders and exhibit autocrine-negative growth response to TGF beta 1. Both lines express TGF beta 1 mRNA at levels 11-12-fold higher than the parental line and respond to exogenous TGF beta 1 by growth inhibition. HD3 cells secrete biologically active TGF beta 1 into conditioned media, which inhibited growth of a TGF beta 1-sensitive mink cell line. This inhibition was blocked by antisera to TGF beta 1, proving the specificity of the inhibition. A range of concentrations of this TGF beta 1 antiserum stimulated HD3 cell growth in a dose-dependent manner, further documenting the autocrine-negative response of the cells to TGF beta 1. Another cell line, HI1, was blocked in enterocytic differentiation. HI1 cells synthesized as much TGF beta 1 mRNA as HD3 and HD4 cells, yet they responded to exogenous TGF beta 1 with less growth inhibition, suggesting some impairment in their response to TGF beta 1. A third class of response to TGF beta 1 was exhibited by the HP1 cell line, which was resistant to HMBA-induced differentiation, remaining undifferentiated with a multilayered growth pattern. HP1 cells synthesized TGF beta 1 mRNA at levels over 20 times the parental level but were stimulated to divide by TGF beta 1, exhibiting autocrine-positive response to this growth factor.(ABSTRACT TRUNCATED AT 400 WORDS)


This article has been cited by other articles:


Home page
Cancer Res.Home page
J. Wang, L. Yang, J. Yang, K. Kuropatwinski, W. Wang, X.-Q. Liu, J. Hauser, and M. G. Brattain
Transforming Growth Factor {beta} Induces Apoptosis through Repressing the Phosphoinositide 3-Kinase/AKT/Survivin Pathway in Colon Cancer Cells
Cancer Res., May 1, 2008; 68(9): 3152 - 3160.
[Abstract] [Full Text] [PDF]


Home page
Am. J. Physiol. Gastrointest. Liver Physiol.Home page
N. S. Belaguli, M. Zhang, M. Rigi, M. Aftab, and D. H. Berger
Cooperation between GATA4 and TGF-beta signaling regulates intestinal epithelial gene expression
Am J Physiol Gastrointest Liver Physiol, June 1, 2007; 292(6): G1520 - G1533.
[Abstract] [Full Text] [PDF]


Home page
J Biol ChemHome page
J. Wang, N. Sergina, T. C. Ko, J. Gong, and M. G. Brattain
Autocrine and Exogenous Transforming Growth Factor {beta} Control Cell Cycle Inhibition through Pathways with Different Sensitivity
J. Biol. Chem., September 17, 2004; 279(38): 40237 - 40244.
[Abstract] [Full Text] [PDF]


Home page
J Biol ChemHome page
G.-Y. Kim, S. E. Mercer, D. Z. Ewton, Z. Yan, K. Jin, and E. Friedman
The Stress-activated Protein Kinases p38{alpha} and JNK1 Stabilize p21Cip1 by Phosphorylation
J. Biol. Chem., August 16, 2002; 277(33): 29792 - 29802.
[Abstract] [Full Text] [PDF]


Home page
Am. J. Physiol. Cell Physiol.Home page
J.-R. Basque, P. Chailler, and D. Menard
Laminins and TGF-{beta} maintain cell polarity and functionality of human gastric glandular epithelium
Am J Physiol Cell Physiol, April 1, 2002; 282(4): C873 - C884.
[Abstract] [Full Text] [PDF]


Home page
J Biol ChemHome page
Z. Yan, G.-Y. Kim, X. Deng, and E. Friedman
Transforming Growth Factor {beta}1 Induces Proliferation in Colon Carcinoma Cells by Ras-dependent, smad-independent Down-regulation of p21cip1
J. Biol. Chem., March 22, 2002; 277(12): 9870 - 9879.
[Abstract] [Full Text] [PDF]


Home page
Cell Growth Differ.Home page
H. Yang, S. Kyo, M. Takatura, and L. Sun
Autocrine Transforming Growth Factor {beta} Suppresses Telomerase Activity and Transcription of Human Telomerase Reverse Transcriptase in Human Cancer Cells
Cell Growth Differ., February 1, 2001; 12(2): 119 - 127.
[Abstract] [Full Text]


Home page
J Biol ChemHome page
Z. Yan, X. Deng, and E. Friedman
Oncogenic Ki-ras Confers a More Aggressive Colon Cancer Phenotype through Modification of Transforming Growth Factor-{beta} Receptor III
J. Biol. Chem., January 12, 2001; 276(2): 1555 - 1563.
[Abstract] [Full Text] [PDF]


Home page
J Biol ChemHome page
J. Yue and K. M. Mulder
Requirement of Ras/MAPK Pathway Activation by Transforming Growth Factor {beta} for Transforming Growth Factor {beta}1Production in a Smad-dependent Pathway
J. Biol. Chem., October 6, 2000; 275(40): 30765 - 30773.
[Abstract] [Full Text] [PDF]


Home page
Cancer Res.Home page
K. Lee, X. Deng, and E. Friedman
Mirk Protein Kinase Is a Mitogen-activated Protein Kinase Substrate That Mediates Survival of Colon Cancer Cells
Cancer Res., July 1, 2000; 60(13): 3631 - 3637.
[Abstract] [Full Text]


Home page
J. Cell Sci.Home page
W. Bursch, K. Hochegger, L. Torok, B. Marian, A. Ellinger, and R. S. Hermann
Autophagic and apoptotic types of programmed cell death exhibit different fates of cytoskeletal filaments
J. Cell Sci., April 1, 2000; 113(7): 1189 - 1198.
[Abstract] [PDF]


Home page
Cell Growth Differ.Home page
X. Deng, S. Bellis, Z. Yan, and E. Friedman
Differential Responsiveness to Autocrine and Exogenous Transforming Growth Factor (TGF) {beta}1 in Cells with Nonfunctional TGF-{beta} Receptor Type III
Cell Growth Differ., January 1, 1999; 10(1): 11 - 18.
[Abstract] [Full Text]


Home page
Proc. Natl. Acad. Sci. USAHome page
S. Zhou, P. Buckhaults, L. Zawel, F. Bunz, G. Riggins, J. Le Dai, S. E. Kern, K. W. Kinzler, and B. Vogelstein
Targeted deletion of Smad4 shows it is required for transforming growth factor {beta} and activin signaling in colorectal cancer cells
PNAS, March 3, 1998; 95(5): 2412 - 2416.
[Abstract] [Full Text] [PDF]


Home page
J Biol ChemHome page
Z. Yan, M.-x. Chen, M. Perucho, and E. Friedman
Oncogenic Ki-ras but Not Oncogenic Ha-rasBlocks Integrin {beta}1-Chain Maturation in Colon Epithelial Cells
J. Biol. Chem., December 5, 1997; 272(49): 30928 - 30936.
[Abstract] [Full Text] [PDF]


Home page
J Biol ChemHome page
Z. Yan, X. Deng, M. Chen, Y. Xu, M. Ahram, B. F. Sloane, and E. Friedman
Oncogenic c-Ki-ras but Not Oncogenic c-Ha-ras Up-regulates CEA Expression and Disrupts Basolateral Polarity in Colon Epithelial Cells
J. Biol. Chem., October 31, 1997; 272(44): 27902 - 27907.
[Abstract] [Full Text] [PDF]


Home page
J Biol ChemHome page
L. Sun and C. Chen
Expression of Transforming Growth Factor {beta} Type III Receptor Suppresses Tumorigenicity of Human Breast Cancer MDA-MB-231 Cells
J. Biol. Chem., October 3, 1997; 272(40): 25367 - 25372.
[Abstract] [Full Text] [PDF]


Home page
J Biol ChemHome page
C. Chen, X.-F. Wang, and L. Sun
Expression of Transforming Growth Factor {beta} (TGF{beta}) Type III Receptor Restores Autocrine TGF{beta}1 Activity in Human Breast Cancer MCF-7 Cells
J. Biol. Chem., May 9, 1997; 272(19): 12862 - 12867.
[Abstract] [Full Text] [PDF]


Home page
J Biol ChemHome page
J. Wang, W. Han, E. Zborowska, J. Liang, X. Wang, J. K. V. Willson, L. Sun, and M. G. Brattain
Reduced Expression of Transforming Growth Factor {beta} Type I Receptor Contributes to the Malignancy of Human Colon Carcinoma Cells
J. Biol. Chem., July 19, 1996; 271(29): 17366 - 17371.
[Abstract] [Full Text] [PDF]


Home page
J Biol ChemHome page
S. Sauma and E. Friedman
Increased Expression of Protein Kinase C Activates ERK3
J. Biol. Chem., May 10, 1996; 271(19): 11422 - 11426.
[Abstract] [Full Text] [PDF]


Home page
J Biol ChemHome page
Y. Zhao and S. L. Young
Requirement of Transforming Growth Factor-{beta} (TGF-{beta}) Type II Receptor for TGF-{beta}-induced Proliferation and Growth Inhibition
J. Biol. Chem., February 2, 1996; 271(5): 2369 - 2372.
[Abstract] [Full Text] [PDF]


Home page
DevelopmentHome page
V. Buchman, M Sporn, and A. Davies
Role of transforming growth factor-beta isoforms in regulating the expression of nerve growth factor and neurotrophin-3 mRNA levels in embryonic cutaneous cells at different stages of development
Development, January 6, 1994; 120(6): 1621 - 1629.
[Abstract] [PDF]


Home page
J. Cell Sci.Home page
T. Lesuffleur, N. Porchet, J. P. Aubert, D. Swallow, J. R. Gum, Y. S. Kim, F. X. Real, and A. Zweibaum
Differential expression of the human mucin genes MUC1 to MUC5 in relation to growth and differentiation of different mucus-secreting HT-29 cell subpopulations
J. Cell Sci., November 1, 1993; 106(3): 771 - 783.
[Abstract] [PDF]


Home page
Cold Spring Harb Symp Quant BiolHome page
L. Hedrick, K.R. Cho, J. Boyd, J. Risinger, and B. Vogelstein
DCC: A Tumor Suppressor Gene Expressed on the Cell Surface
Cold Spring Harb Symp Quant Biol, January 1, 1992; 57(0): 345 - 351.
[Abstract] [PDF]


Home page
J Biol ChemHome page
J. Yue and K. M. Mulder
Requirement of Ras/MAPK Pathway Activation by Transforming Growth Factor {beta} for Transforming Growth Factor {beta}1Production in a Smad-dependent Pathway
J. Biol. Chem., October 6, 2000; 275(40): 30765 - 30773.
[Abstract] [Full Text] [PDF]


Home page
J Biol ChemHome page
Z. Yan, X. Deng, and E. Friedman
Oncogenic Ki-ras Confers a More Aggressive Colon Cancer Phenotype through Modification of Transforming Growth Factor-{beta} Receptor III
J. Biol. Chem., January 12, 2001; 276(2): 1555 - 1563.
[Abstract] [Full Text] [PDF]


Home page
Am. J. Physiol. Cell Physiol.Home page
J.-R. Basque, P. Chailler, and D. Menard
Laminins and TGF-{beta} maintain cell polarity and functionality of human gastric glandular epithelium
Am J Physiol Cell Physiol, April 1, 2002; 282(4): C873 - C884.
[Abstract] [Full Text] [PDF]




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Cancer Research Clinical Cancer Research
Cancer Epidemiology Biomarkers & Prevention Molecular Cancer Therapeutics
Molecular Cancer Research Cell Growth & Differentiation
Copyright © 1990 by the American Association of Cancer Research.