| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
Carcinogenesis |
Laboratory of Cellular Carcinogenesis and Tumor Promotion, National Cancer Institute, Bethesda, Maryland 20892-4255
Treatment of estrogen receptor (ER)-positive MCF-7 human breast cancer cells with retinoic acid (RA) inhibited cell growth and increased cell adhesion to fibronectin. In contrast, ER- MDA-MB-231 cells failed to respond. Western blot analysis showed that tyrosine phosphorylation of two major bands at Mr 125,000 and Mr 68,000 was induced by RA in ER+ MCF-7 human breast carcinoma cells. However, this induction was a late phenomenon detectable at 12 and 24 h, but not within 3 h. A similar increase of tyrosine phosphorylation by RA was observed in ER+ human breast cancer cell lines T-47D and ZR-75-1, but not in the ER- cell lines MDA-MB-231, MDA-MB-453, and MDA-MB-468. Focal adhesion kinase and paxillin, which localize in focal adhesion plaques and may play important roles in the integrin signaling pathway, were identified as the major proteins showing RA-induced tyrosine phosphorylation. The retinoid X receptor-selective compound SR11237 failed to induce tyrosine phosphorylation, indicating that retinoid X receptor activation is not involved in this phenomenon. In contrast, stable overexpression of a truncated RA receptor (RAR) 
cDNA, RAR403, with strong RAR dominant negative activity prevented the increase in tyrosine phosphate, suggesting that RAR signaling is involved in RA-induced tyrosine phosphorylation. Tyrosine phosphorylation was induced the most by the RAR- (193836), followed by RAR-
(194433), but was not significantly induced by RAR-ß (193174)-selective retinoids. This study demonstrates a coordinated albeit relatively late effect of RA on cell adhesion and tyrosine phosphorylation in ER+ human breast cancer cells and suggests RAR- as the major responsible retinoid receptor.
This article has been cited by other articles:
|
|
 |
|
  A. Gattelli, M. N. Zimberlin, R. P. Meiss, L. H. Castilla, and E. C. Kordon Selection of Early-Occurring Mutations Dictates Hormone-Independent Progression in Mouse Mammary Tumor Lines J. Virol., November 15, 2006; 80(22): 11409 - 11415. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 C. Rousseau, J. N. Nichol, F. Pettersson, M.-C. Couture, and W. H. Miller Jr. ER{beta} Sensitizes Breast Cancer Cells to Retinoic Acid: Evidence of Transcriptional Crosstalk Mol. Cancer Res., September 1, 2004; 2(9): 523 - 531. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 C. M. Karp, H. Pan, M. Zhang, D. J. Buckley, L. A. Schuler, and A. R. Buckley Identification of HRPAP20: A Novel Phosphoprotein that Enhances Growth and Survival in Hormone-Responsive Tumor Cells Cancer Res., February 1, 2004; 64(3): 1016 - 1025. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. A. Antonyak, J. E. Boehm, and R. A. Cerione Phosphoinositide 3-Kinase Activity Is Required for Retinoic Acid-induced Expression and Activation of the Tissue Transglutaminase J. Biol. Chem., April 19, 2002; 277(17): 14712 - 14716. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 A. Watanabe, M. Kurabayashi, M. Arai, K. Sekiguchi, and R. Nagai Combined effect of retinoic acid and basic FGF on PAI-1 gene expression in vascular smooth muscle cells Cardiovasc Res, July 1, 2001; 51(1): 151 - 159. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 K. Fukunaka, T. Saito, K. Wataba, K. Ashihara, E. Ito, and R. Kudo Changes in expression and subcellular localization of nuclear retinoic acid receptors in human endometrial epithelium during the menstrual cycle Mol. Hum. Reprod., May 1, 2001; 7(5): 437 - 446. [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 |
