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Title: Synergistic effects of retinoic acid and tamoxifen on human breast cancer cells: Proteomic characterization

Journal Article · · Experimental Cell Research
 [1];  [1];  [2];  [3]
  1. Department of Chemistry, University of Hong Kong, Pokfulam, Hong Kong (China)
  2. Department of Biochemistry, University of Vermont, College of Medicine, Burlington 05405 (United States)
  3. Department of Anatomy, The University of Hong Kong, Pokfulam, Hong Kong (China) and Department of Biochemistry, University of Vermont, College of Medicine, Burlington 05405 (United States)

The anti-estrogen tamoxifen and vitamin A-related compound, all-trans retinoic acid (RA), in combination act synergistically to inhibit the growth of MCF-7 human breast cancer cells. In the present study, we applied two-dimensional gel electrophoresis based proteomic approach to globally analyze this synergistic effect of RA and tamoxifen. Proteomic study revealed that multiple clusters of proteins were involved in RA and tamoxifen-induced apoptosis in MCF-7 breast cancer cells, including post-transcriptional and splicing factors, proteins related to cellular proliferation or differentiation, and proteins related to energy production and internal degradation systems. The negative growth factor-transforming growth factor {beta} (TGF{beta}) was secreted by RA and/or tamoxifen treatment and was studies as a potential mediator of the synergistic effects of RA and tamoxifen in apoptosis. By comparing protein alterations in treatments of RA and tamoxifen alone or in combination to those of TGF{beta} treatment, or co-treatment with TGF{beta} inhibitor SB 431542, proteomic results showed that a number of proteins were involved in TGF{beta} signaling pathway. These results provide valuable insights into the mechanisms of RA and tamoxifen-induced TGF{beta} signaling pathway in breast cancer cells.

OSTI ID:
20972107
Journal Information:
Experimental Cell Research, Vol. 313, Issue 2; Other Information: DOI: 10.1016/j.yexcr.2006.10.016; PII: S0014-4827(06)00442-3; Copyright (c) 2006 Elsevier Science B.V., Amsterdam, The Netherlands, All rights reserved; Country of input: International Atomic Energy Agency (IAEA); ISSN 0014-4827
Country of Publication:
United States
Language:
English