Proliferation and metastatic potential of endometrial cancer cells in response to metformin treatment in a high versus normal glucose environment
Autor(a) principal: | |
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Data de Publicação: | 2016 |
Outros Autores: | , , , , , , , |
Tipo de documento: | Artigo |
Idioma: | eng |
Título da fonte: | Repositório Institucional da UFRGS |
Texto Completo: | http://hdl.handle.net/10183/150412 |
Resumo: | In order to improve our understanding of the potential preventive and therapeutic role of metformin, the present study aimed to investigate the capability of low-dose metformin in the efficient inhibition of cancer development and the reduction of the metastasis of endometrial adenocarcinoma type I and primary endometrial epithelial cells (eEPs), with the drug acting as a treatment in a hyperinsulinemic environment exposed to high and normal glucose conditions. The Ishikawa endometrial adenocarcinoma cell line and primary eEPs were exposed to an environment with high (17 mM) or normal glucose (5 mM) and treated with insulin, low-dose metformin (0.1 mM) or a combined treatment. Metastatic potential was assessed by migration and invasion assays, and relative cell proliferation was determined. Metformin at a low dose potently inhibited the insulin action, decreasing the ability of the endometrial cancer (EC) cell line to migrate and invade in a high and normal glucose environment, and decreasing the migration ability of the primary eEPs. In the EC cell line, the insulin treatment increased the proliferation, without any subsequent reduction of proliferation by the addition of 0.1 mM metformin; however, relative cell proliferation sensitivity to metformin was observed in the range between 1 and 5 mM regardless of the glucose concentration present. Overall, metformin at 0.1 mM is not efficient enough to decrease the proliferation in an EC cell line. However, at this concentration, metformin can inhibit the insulin action in endometrial epithelial cancer cells, demonstrating an anti-metastatic effect in high and normal glucose environments. |
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Machado, Amanda de BarrosReis, Vania Marisia Santos Fortes dosWeber, SebastianJauckus, JuliaBrum, Ilma SimoniCorleta, Helena von EyeStrowitzki, ThomasCapp, EdisonGermeyer, Ariane2017-01-04T02:26:53Z20161792-1082http://hdl.handle.net/10183/150412001007975In order to improve our understanding of the potential preventive and therapeutic role of metformin, the present study aimed to investigate the capability of low-dose metformin in the efficient inhibition of cancer development and the reduction of the metastasis of endometrial adenocarcinoma type I and primary endometrial epithelial cells (eEPs), with the drug acting as a treatment in a hyperinsulinemic environment exposed to high and normal glucose conditions. The Ishikawa endometrial adenocarcinoma cell line and primary eEPs were exposed to an environment with high (17 mM) or normal glucose (5 mM) and treated with insulin, low-dose metformin (0.1 mM) or a combined treatment. Metastatic potential was assessed by migration and invasion assays, and relative cell proliferation was determined. Metformin at a low dose potently inhibited the insulin action, decreasing the ability of the endometrial cancer (EC) cell line to migrate and invade in a high and normal glucose environment, and decreasing the migration ability of the primary eEPs. In the EC cell line, the insulin treatment increased the proliferation, without any subsequent reduction of proliferation by the addition of 0.1 mM metformin; however, relative cell proliferation sensitivity to metformin was observed in the range between 1 and 5 mM regardless of the glucose concentration present. Overall, metformin at 0.1 mM is not efficient enough to decrease the proliferation in an EC cell line. However, at this concentration, metformin can inhibit the insulin action in endometrial epithelial cancer cells, demonstrating an anti-metastatic effect in high and normal glucose environments.application/pdfengOncology letters. Athens, Greece. Vol. 12, no. 5 (Nov. 2016), p. 3626–3632Neoplasias do endométrioMetástase neoplásicaMetforminaEndometrial cancerMetforminHyperinsulinemiaGlucoseMetastasisCancer developmentProliferation and metastatic potential of endometrial cancer cells in response to metformin treatment in a high versus normal glucose environmentEstrangeiroinfo:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/openAccessreponame:Repositório Institucional da UFRGSinstname:Universidade Federal do Rio Grande do Sul (UFRGS)instacron:UFRGSORIGINAL001007975.pdf001007975.pdfTexto completo (inglês)application/pdf472609http://www.lume.ufrgs.br/bitstream/10183/150412/1/001007975.pdfb3f1c3291d53440f3743f75e4dbff9ccMD51TEXT001007975.pdf.txt001007975.pdf.txtExtracted Texttext/plain33307http://www.lume.ufrgs.br/bitstream/10183/150412/2/001007975.pdf.txt6af077bf30c01fa65171cfa601c084adMD52THUMBNAIL001007975.pdf.jpg001007975.pdf.jpgGenerated Thumbnailimage/jpeg2179http://www.lume.ufrgs.br/bitstream/10183/150412/3/001007975.pdf.jpg495b13db70834bbfb280f01955690d0fMD5310183/1504122023-05-13 03:28:33.728578oai:www.lume.ufrgs.br:10183/150412Repositório de PublicaçõesPUBhttps://lume.ufrgs.br/oai/requestopendoar:2023-05-13T06:28:33Repositório Institucional da UFRGS - Universidade Federal do Rio Grande do Sul (UFRGS)false |
dc.title.pt_BR.fl_str_mv |
Proliferation and metastatic potential of endometrial cancer cells in response to metformin treatment in a high versus normal glucose environment |
title |
Proliferation and metastatic potential of endometrial cancer cells in response to metformin treatment in a high versus normal glucose environment |
spellingShingle |
Proliferation and metastatic potential of endometrial cancer cells in response to metformin treatment in a high versus normal glucose environment Machado, Amanda de Barros Neoplasias do endométrio Metástase neoplásica Metformina Endometrial cancer Metformin Hyperinsulinemia Glucose Metastasis Cancer development |
title_short |
Proliferation and metastatic potential of endometrial cancer cells in response to metformin treatment in a high versus normal glucose environment |
title_full |
Proliferation and metastatic potential of endometrial cancer cells in response to metformin treatment in a high versus normal glucose environment |
title_fullStr |
Proliferation and metastatic potential of endometrial cancer cells in response to metformin treatment in a high versus normal glucose environment |
title_full_unstemmed |
Proliferation and metastatic potential of endometrial cancer cells in response to metformin treatment in a high versus normal glucose environment |
title_sort |
Proliferation and metastatic potential of endometrial cancer cells in response to metformin treatment in a high versus normal glucose environment |
author |
Machado, Amanda de Barros |
author_facet |
Machado, Amanda de Barros Reis, Vania Marisia Santos Fortes dos Weber, Sebastian Jauckus, Julia Brum, Ilma Simoni Corleta, Helena von Eye Strowitzki, Thomas Capp, Edison Germeyer, Ariane |
author_role |
author |
author2 |
Reis, Vania Marisia Santos Fortes dos Weber, Sebastian Jauckus, Julia Brum, Ilma Simoni Corleta, Helena von Eye Strowitzki, Thomas Capp, Edison Germeyer, Ariane |
author2_role |
author author author author author author author author |
dc.contributor.author.fl_str_mv |
Machado, Amanda de Barros Reis, Vania Marisia Santos Fortes dos Weber, Sebastian Jauckus, Julia Brum, Ilma Simoni Corleta, Helena von Eye Strowitzki, Thomas Capp, Edison Germeyer, Ariane |
dc.subject.por.fl_str_mv |
Neoplasias do endométrio Metástase neoplásica Metformina |
topic |
Neoplasias do endométrio Metástase neoplásica Metformina Endometrial cancer Metformin Hyperinsulinemia Glucose Metastasis Cancer development |
dc.subject.eng.fl_str_mv |
Endometrial cancer Metformin Hyperinsulinemia Glucose Metastasis Cancer development |
description |
In order to improve our understanding of the potential preventive and therapeutic role of metformin, the present study aimed to investigate the capability of low-dose metformin in the efficient inhibition of cancer development and the reduction of the metastasis of endometrial adenocarcinoma type I and primary endometrial epithelial cells (eEPs), with the drug acting as a treatment in a hyperinsulinemic environment exposed to high and normal glucose conditions. The Ishikawa endometrial adenocarcinoma cell line and primary eEPs were exposed to an environment with high (17 mM) or normal glucose (5 mM) and treated with insulin, low-dose metformin (0.1 mM) or a combined treatment. Metastatic potential was assessed by migration and invasion assays, and relative cell proliferation was determined. Metformin at a low dose potently inhibited the insulin action, decreasing the ability of the endometrial cancer (EC) cell line to migrate and invade in a high and normal glucose environment, and decreasing the migration ability of the primary eEPs. In the EC cell line, the insulin treatment increased the proliferation, without any subsequent reduction of proliferation by the addition of 0.1 mM metformin; however, relative cell proliferation sensitivity to metformin was observed in the range between 1 and 5 mM regardless of the glucose concentration present. Overall, metformin at 0.1 mM is not efficient enough to decrease the proliferation in an EC cell line. However, at this concentration, metformin can inhibit the insulin action in endometrial epithelial cancer cells, demonstrating an anti-metastatic effect in high and normal glucose environments. |
publishDate |
2016 |
dc.date.issued.fl_str_mv |
2016 |
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2017-01-04T02:26:53Z |
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1792-1082 |
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001007975 |
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http://hdl.handle.net/10183/150412 |
dc.language.iso.fl_str_mv |
eng |
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dc.relation.ispartof.pt_BR.fl_str_mv |
Oncology letters. Athens, Greece. Vol. 12, no. 5 (Nov. 2016), p. 3626–3632 |
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openAccess |
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