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Estradiol and progesterone regulate proliferation and apoptosis in colon cancer
Epidemiological studies describe estrogens as protectors in the development of colon cancer in postmenopausal women treated with hormone replacement therapy. However, the role of progesterone in colon cancer has been minimally studied and the results are controversial. For the above, the objective o...
Autores principales: | , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Bioscientifica Ltd
2019
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6391933/ https://www.ncbi.nlm.nih.gov/pubmed/30738018 http://dx.doi.org/10.1530/EC-18-0374 |
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author | Sasso, Corina Verónica Santiano, Flavia Eliana Campo Verde Arboccó, Fiorella Zyla, Leila Esther Semino, Silvana Noemí Guerrero-Gimenez, Martin Eduardo Pistone Creydt, Virginia López Fontana, Constanza Matilde Carón, Rubén Walter |
author_facet | Sasso, Corina Verónica Santiano, Flavia Eliana Campo Verde Arboccó, Fiorella Zyla, Leila Esther Semino, Silvana Noemí Guerrero-Gimenez, Martin Eduardo Pistone Creydt, Virginia López Fontana, Constanza Matilde Carón, Rubén Walter |
author_sort | Sasso, Corina Verónica |
collection | PubMed |
description | Epidemiological studies describe estrogens as protectors in the development of colon cancer in postmenopausal women treated with hormone replacement therapy. However, the role of progesterone in colon cancer has been minimally studied and the results are controversial. For the above, the objective of this work was to determine the hormonal regulation exerted by natural ovarian steroids on proliferation and apoptosis in an experimental model of colon cancer in ovariectomized rats treated with 17-beta estradiol and progesterone. Sprague–Dawley rats were exposed to the carcinogen 1,2-dimethylhydrazine to induce colon tumors. Thirty days later, the rats were ovariectomized and treated with estradiol (60 μg/kg), progesterone (10 mg/kg), estradiol plus progesterone (60 μg/kg and 10 mg/kg) or vehicle. We observed no significant differences in colon cancer incidence and tumor multiplicity between the groups. Nevertheless, we observed a decrease in PCNA expression and a greater number of apoptotic index, higher expression of caspase 3, cleaved PARP and cleaved caspase 8 in tumors, confirming the activation of the extrinsic pathway of apoptosis by the combined treatment. In addition, we observed a higher expression of estrogen receptor beta in these tumors. We conclude that the action of both hormones, estradiol and progesterone, is necessary to reduce proliferation and increase apoptosis in colon tumors, probably through estrogen receptor beta activation. |
format | Online Article Text |
id | pubmed-6391933 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2019 |
publisher | Bioscientifica Ltd |
record_format | MEDLINE/PubMed |
spelling | pubmed-63919332019-03-05 Estradiol and progesterone regulate proliferation and apoptosis in colon cancer Sasso, Corina Verónica Santiano, Flavia Eliana Campo Verde Arboccó, Fiorella Zyla, Leila Esther Semino, Silvana Noemí Guerrero-Gimenez, Martin Eduardo Pistone Creydt, Virginia López Fontana, Constanza Matilde Carón, Rubén Walter Endocr Connect Research Epidemiological studies describe estrogens as protectors in the development of colon cancer in postmenopausal women treated with hormone replacement therapy. However, the role of progesterone in colon cancer has been minimally studied and the results are controversial. For the above, the objective of this work was to determine the hormonal regulation exerted by natural ovarian steroids on proliferation and apoptosis in an experimental model of colon cancer in ovariectomized rats treated with 17-beta estradiol and progesterone. Sprague–Dawley rats were exposed to the carcinogen 1,2-dimethylhydrazine to induce colon tumors. Thirty days later, the rats were ovariectomized and treated with estradiol (60 μg/kg), progesterone (10 mg/kg), estradiol plus progesterone (60 μg/kg and 10 mg/kg) or vehicle. We observed no significant differences in colon cancer incidence and tumor multiplicity between the groups. Nevertheless, we observed a decrease in PCNA expression and a greater number of apoptotic index, higher expression of caspase 3, cleaved PARP and cleaved caspase 8 in tumors, confirming the activation of the extrinsic pathway of apoptosis by the combined treatment. In addition, we observed a higher expression of estrogen receptor beta in these tumors. We conclude that the action of both hormones, estradiol and progesterone, is necessary to reduce proliferation and increase apoptosis in colon tumors, probably through estrogen receptor beta activation. Bioscientifica Ltd 2019-02-04 /pmc/articles/PMC6391933/ /pubmed/30738018 http://dx.doi.org/10.1530/EC-18-0374 Text en © 2019 The authors http://creativecommons.org/licenses/by/4.0/ This work is licensed under a Creative Commons Attribution 4.0 International License. (http://creativecommons.org/licenses/by/4.0/) |
spellingShingle | Research Sasso, Corina Verónica Santiano, Flavia Eliana Campo Verde Arboccó, Fiorella Zyla, Leila Esther Semino, Silvana Noemí Guerrero-Gimenez, Martin Eduardo Pistone Creydt, Virginia López Fontana, Constanza Matilde Carón, Rubén Walter Estradiol and progesterone regulate proliferation and apoptosis in colon cancer |
title | Estradiol and progesterone regulate proliferation and apoptosis in colon cancer |
title_full | Estradiol and progesterone regulate proliferation and apoptosis in colon cancer |
title_fullStr | Estradiol and progesterone regulate proliferation and apoptosis in colon cancer |
title_full_unstemmed | Estradiol and progesterone regulate proliferation and apoptosis in colon cancer |
title_short | Estradiol and progesterone regulate proliferation and apoptosis in colon cancer |
title_sort | estradiol and progesterone regulate proliferation and apoptosis in colon cancer |
topic | Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6391933/ https://www.ncbi.nlm.nih.gov/pubmed/30738018 http://dx.doi.org/10.1530/EC-18-0374 |
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