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 Kitadai, Y.
Right arrow Articles by Tahara, E.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Kitadai, Y.
Right arrow Articles by Tahara, E.

Cell Growth & Differentiation, Vol 4, Issue 4 291-296, Copyright © 1993 by American Association of Cancer Research


ARTICLES

GC factor represses transcription of several growth factor/receptor genes and causes growth inhibition of human gastric carcinoma cell lines

Y Kitadai, H Yamazaki, W Yasui, E Kyo, H Yokozaki, G Kajiyama, AC Johnson, I Pastan and E Tahara
First Department of Pathology, Hiroshima University, School of Medicine, Japan.

The GC factor (GCF) binds to specific GC-rich sequences in the epidermal growth factor receptor (EGFR) gene promoter and represses its transcription. In this study, by the use of GCF transfection, we examined whether GCF represses the gene expression of several other growth factors and receptors and causes growth inhibition of cancer cells. The transfection of GCF expression vector into gastric carcinoma cell lines (TMK-1 and MKN-28) decreased the mRNA levels of transforming growth factor (TGF) alpha, insulin-like growth factor II, and c-met. The reduction of TGF-alpha expression was confirmed at the protein level by enzyme-linked immunosorbent assay. Transfection of GCF expression vector interfered with the mRNA accumulation for EGFR and TGF-beta induced by epidermal growth factor in gastric carcinoma cell lines. The carcinoma cells transfected with GCF expression vector did not grow in a serum-free medium, whereas the control cells did grow under serum-free conditions. When the growth of the gastric carcinoma cell lines was studied in nude mice, GCF-transfected carcinoma cells showed a significantly slower growth compared to the control tumor. Transient cotransfection analysis with NIH3T3 cells revealed that GCF repressed the promoter activity of TGF-alpha in addition to EGFR. These findings indicate that GCF negatively regulates gene expression of not only the EGFR but also several other growth factor and receptor genes and can inhibit the growth of gastric carcinomas in immunodeficient mice.


This article has been cited by other articles:


Home page
J Biol ChemHome page
A. L. Reed, H. Yamazaki, J. D. Kaufman, Y. Rubinstein, B. Murphy, and A. C. Johnson
Molecular Cloning and Characterization of a Transcription Regulator with Homology to GC-binding Factor
J. Biol. Chem., August 21, 1998; 273(34): 21594 - 21602.
[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 © 1993 by the American Association of Cancer Research.