Human endometrial carcinoma cells release factors which inhibit the growth of normal epithelial cells in culture |
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Authors: | C D Albright G J Tsongalis J H Resau D G Kaufman |
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Institution: | (1) Department of Pathology, School of Medicine, The University of North Carolina, McGavran-Greenberg Hall, CB#7400, 27599 Chapel Hill, North Carolina, USA;(2) Present address: Department of Nutrition, School of Public Health, The University of North Carolina, North Carolina, USA;(3) Present address: Associate Division of Clinical Chemistry, Hartford Hospital, 208 Seymour Street, Hartford, Connecticut, USA;(4) Department of Pathology, University of Maryland School of Medicine, Baltimore, Maryland, USA;(5) Present address: NCI-FCRDC ABL, Frederick, Maryland, USA |
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Abstract: | Autocrine and paracrine interactions between cells are important homeostatic mediators in normal tissues. Alterations to growth factor signalling pathways are likely to play a role in multistep carcinogenesis. In this study normal human endometrial epithelial cells (NHEC) after 3 days in culture were treated with serum-free medium conditioned for 24 h by log phase or confluent cultures of established RL95-2, HEC1A, or AN3CA endometrial carcinoma (EC) cell lines. By day 4, NHEC treated with either log phase or confluent conditioned medium (CM) showed a significant decrease (50–90% of control) in 3H]thymidine (3H]TdR) incorporation. DNA synthesis was inhibited more by confluent than by log phase CM. By day 7, NHEC treated with CM exhibited fewer colonies per culture, fewer cells per colony, and an increased percentage of single cells. Several growth-regulatory gene products found in the nucleus or at the cell membrane have been shown to be expressed differently in normal and transformed cells. We selected the p53 and c-Ha-ras p21 proteins to further investigate the mechanism of alteration of proliferation in cells treated with carcinoma CM. Thus, by day 7, the percentage of NHEC with nuclear localization of wild type p53 (wt p53) was elevated by treatment with CM. In contrast, CM-treated EC cells continued to proliferate, and showed a decrease in the percentage of cells expressing nuclear wt p53 and an increase in the cytoplasmic expression of c-Ha-ras p21. Our studies show that EC cell lines release factors which inhibit the proliferation of NHEC, thus favoring the proliferation of EC cells.Abbreviations CM
conditioned medium
- EC
endometrial adenocarcinoma
- NHEC
normal human endometrial epithelial cells |
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Keywords: | communication endometrial carcinoma epithelial cells growth factors |
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