Cancer Research Cancer Epigenetics  EMT and Cancer Progression and Treatment
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Cancer Research Clinical Cancer Research
Cancer Epidemiology Biomarkers & Prevention Molecular Cancer Therapeutics
Molecular Cancer Research Cancer Prevention Research
Cancer Prevention Journals Portal Cancer Reviews Online
Annual Meeting Education Book Meeting Abstracts Online

[Cancer Research 51, 4882-4887, September 15, 1991]
© 1991 American Association for Cancer Research

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 Email this article to a friend
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 reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Crouch, G. D.
Right arrow Articles by Helman, L. J.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Crouch, G. D.
Right arrow Articles by Helman, L. J.

All-trans-retinoic Acid Inhibits the Growth of Human Rhabdomyosarcoma Cell Lines

Gary D. Crouch and Lee J. Helman1

Molecular Genetics Section, Pediatric Branch, National Cancer Institute, Bethesda, Maryland 20892

We have been evaluating the role of all-trans-retinoic acid (RA) in the differentiation and growth of human rhabdomyosarcoma (RMS) cell lines. Treatment of both embryonal (RD) and alveolar (RH30) human RMS cell lines with all-trans-RA resulted in a dose-dependent inhibition of cell growth with a maximal inhibition of 92 and 66%, respectively, at 5 x 10-6 M. When 13-cis-RA was used under identical experimental conditions, maximal growth inhibition was 41 and 37%, respectively. This stereo-specific growth inhibition was not associated with morphological or biochemical evidence of myogenic differentiation. Furthermore, all-trans-RA demonstrated no evidence of competition with binding of insulin-like growth factor II (IGF-II), an autocrine growth factor in RMS, to its membrane receptor as evaluated by an [125I]IGF-I receptor-binding assay. Attempts to rescue all-trans-RA growth-inhibited RMS cells with exogenous IGF-II resulted in no increase in growth compared to cells treated with all-trans-RA alone. We conclude that RA inhibits the growth of human RMS cell lines in a dose-dependent, stereo-specific manner, is not associated with differentiation, and does not appear to be directly related to IGF-II.

1 To whom requests for reprints should be addressed, at Molecular Genetics Section, Pediatric Branch, National Cancer Institute, Building 10, Room 13N240, Bethesda, MD 20892.

Received 3/12/91. Accepted 7/ 8/91.




This article has been cited by other articles:


Home page
Mol. Biol. CellHome page
O. Ostrovsky, N. T. Ahmed, and Y. Argon
The Chaperone Activity of GRP94 Toward Insulin-like Growth Factor II Is Necessary for the Stress Response to Serum Deprivation
Mol. Biol. Cell, March 15, 2009; 20(6): 1855 - 1864.
[Abstract] [Full Text] [PDF]


Home page
Drug Metab. Dispos.Home page
G. S. Gorman, L. Coward, C. Kerstner-Wood, L. Cork, I. M. Kapetanovic, W. J. Brouillette, and D. D. Muccio
In Vitro Metabolic Characterization, Phenotyping, and Kinetic Studies of 9cUAB30, a Retinoid X Receptor-Specific Retinoid
Drug Metab. Dispos., July 1, 2007; 35(7): 1157 - 1164.
[Abstract] [Full Text] [PDF]


Home page
Mol Cancer ResHome page
D. L. Crowe, R. Kim, and R. A.S. Chandraratna
Retinoic Acid Differentially Regulates Cancer Cell Proliferation via Dose-Dependent Modulation of the Mitogen-Activated Protein Kinase Pathway
Mol. Cancer Res., May 1, 2003; 1(7): 532 - 540.
[Abstract] [Full Text] [PDF]


Home page
Clin. Cancer Res.Home page
P. C. Adamson, B. C. Widemann, G. H. Reaman, N. L. Seibel, R. F. Murphy, A. F. Gillespie, and F. M. Balis
A Phase I Trial and Pharmacokinetic Study of 9-cis-Retinoic Acid (ALRT1057) in Pediatric Patients with Refractory Cancer: A Joint Pediatric Oncology Branch, National Cancer Institute, and Children's Cancer Group Study
Clin. Cancer Res., October 1, 2001; 7(10): 3034 - 3039.
[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 Cancer Prevention Research
Cancer Prevention Journals Portal Cancer Reviews Online
Annual Meeting Education Book Meeting Abstracts Online
Copyright © 1991 by the American Association for Cancer Research.