Journal
JOURNAL OF THE CHINESE MEDICAL ASSOCIATION
Volume 76, Issue 2, Pages 63-70Publisher
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1016/j.jcma.2012.08.023
Keywords
cell-cycle regulatory proteins; cell line; estrogen; ovarian cancer
Categories
Funding
- Taipei Veterans General Hospital, Taipei, Taiwan [V99C1-085, V100C-054, V100C-185, V101A-035, V101C1-128, V101E4-004, V101E5-006]
- foundation of Chao Shao-Kang, Taipei, Taiwan
- National Science Council, Taipei, Taiwan [NSC 96-2314-B-010-018-MY3, NSC 99-2314-B-010-009-MY3]
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Background: The role of estrogen in the growth and survival of ovarian cancer cells is controversial. In this study, we investigated the changes in cell-cycle regulatory proteins in ovarian cancer cell lines after estrogen treatment to explore the role of estrogen in ovarian cancers. Methods: Two ovarian adenocarcinoma cell lines were used for the study: the first, OC-117-VGH, was deficient in estrogen receptors (ER)alpha and ER beta, and the second, OVCAR3, was positive for ER alpha and ER beta. Serial concentrations of estrogen were used to evaluate the effects of estrogen on the survival of ovarian cancer cells. The cell-cycle regulatory proteins, including cyclin D1, cyclin E, p16/INK4a, and p27/KIP1, were used to check the possible mechanism of an estrogen effect on survival of the cancer cell line. Results: Estrogen 0.01-1.0 mu M inhibited the growth of both cell lines. There were no differences in cyclin D1 and E expression between the two cell lines after estrogen treatment, but the expression of p16/INK4a and p27/KIP1 was significantly higher in the OC-1170-VGH cell line than in the OVCAR3 cell line. Conclusion: Although the ER-positive and ER-negative ovarian cancer cell lines were inhibited by estrogen, the influence of cell-cycle regulatory proteins was different between the two, suggesting that the inhibitory effect of estrogen on ovarian cancer cell lines might be mediated through different pathways. Copyright (c) 2012 Elsevier Taiwan LLC and the Chinese Medical Association. All rights reserved.
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