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Curcumin for the Prevention of Epithelial-Mesenchymal Transition in Endoxifen-Treated MCF-7 Breast Cancer Cells

BACKGROUND: Curcumin was shown to reduce epithelial-mesenchymal transition (EMT) markers in previous short term studies. This study was aimed to investigate the potential of curcumin in the prevention of EMT activation in MCF-7 cells induced by endoxifen. METHODS: MCF-7 breast cancer cells were trea...

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Autores principales: Paramita, P, Wardhani, Bantari WK, Wanandi, Septelia Inawati, Louisa, Melva
Formato: Online Artículo Texto
Lenguaje:English
Publicado: West Asia Organization for Cancer Prevention 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6031844/
https://www.ncbi.nlm.nih.gov/pubmed/29801408
http://dx.doi.org/10.22034/APJCP.2018.19.5.1243
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author Paramita, P
Wardhani, Bantari WK
Wanandi, Septelia Inawati
Louisa, Melva
author_facet Paramita, P
Wardhani, Bantari WK
Wanandi, Septelia Inawati
Louisa, Melva
author_sort Paramita, P
collection PubMed
description BACKGROUND: Curcumin was shown to reduce epithelial-mesenchymal transition (EMT) markers in previous short term studies. This study was aimed to investigate the potential of curcumin in the prevention of EMT activation in MCF-7 cells induced by endoxifen. METHODS: MCF-7 breast cancer cells were treated with Endoxifen 1000 nM+beta-estradiol 1 nM with or without curcumin (8.5µM or 17 µM). Cells treated with dimethyl sulfoxide (DMSO) 0.001% were used as negative control. After 8 weeks of continuous treatment, the cells were counted, analyzed for mRNA E-cadherin, vimentin, TGF-β expression, total reactive oxygen species (ROS) and observed for morphological changes using confocal microscope and transmission electron microscope. RESULT: MCF-7 cell viability was increased in endoxifen + β-estradiol group. Cell viability was significantly decreased in curcumin 17 µM, but not in curcumin 8.5 µM group. Analysis of EMT markers at week 8 indicates that there were increase in vimentin and TGF-β mRNA expressions, while E-cadherin mRNA expressions and TGF-β1 protein concentrations were shown to decrease. The results showed that administration of curcumin in all the dose administered were incapable improving the expressions of vimentin, TGF-β1 and E-cadherin. There was a decrease in ROS concentration in curcumin treated cells (8.5 µM) while in curcumin 17 µM, ROS concentration was increased. Morphological observation using confocal microscope and TEM showed the presence of mesenchymal cells and adherens junction. CONCLUSION: endoxifen treatments for eight weeks resulted in upregulation of EMT markers and changes in morphology of MCF-7 breast cancer cells. The addition of curcumin did not prevent the activation of EMT.
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spelling pubmed-60318442018-07-11 Curcumin for the Prevention of Epithelial-Mesenchymal Transition in Endoxifen-Treated MCF-7 Breast Cancer Cells Paramita, P Wardhani, Bantari WK Wanandi, Septelia Inawati Louisa, Melva Asian Pac J Cancer Prev Research Article BACKGROUND: Curcumin was shown to reduce epithelial-mesenchymal transition (EMT) markers in previous short term studies. This study was aimed to investigate the potential of curcumin in the prevention of EMT activation in MCF-7 cells induced by endoxifen. METHODS: MCF-7 breast cancer cells were treated with Endoxifen 1000 nM+beta-estradiol 1 nM with or without curcumin (8.5µM or 17 µM). Cells treated with dimethyl sulfoxide (DMSO) 0.001% were used as negative control. After 8 weeks of continuous treatment, the cells were counted, analyzed for mRNA E-cadherin, vimentin, TGF-β expression, total reactive oxygen species (ROS) and observed for morphological changes using confocal microscope and transmission electron microscope. RESULT: MCF-7 cell viability was increased in endoxifen + β-estradiol group. Cell viability was significantly decreased in curcumin 17 µM, but not in curcumin 8.5 µM group. Analysis of EMT markers at week 8 indicates that there were increase in vimentin and TGF-β mRNA expressions, while E-cadherin mRNA expressions and TGF-β1 protein concentrations were shown to decrease. The results showed that administration of curcumin in all the dose administered were incapable improving the expressions of vimentin, TGF-β1 and E-cadherin. There was a decrease in ROS concentration in curcumin treated cells (8.5 µM) while in curcumin 17 µM, ROS concentration was increased. Morphological observation using confocal microscope and TEM showed the presence of mesenchymal cells and adherens junction. CONCLUSION: endoxifen treatments for eight weeks resulted in upregulation of EMT markers and changes in morphology of MCF-7 breast cancer cells. The addition of curcumin did not prevent the activation of EMT. West Asia Organization for Cancer Prevention 2018 /pmc/articles/PMC6031844/ /pubmed/29801408 http://dx.doi.org/10.22034/APJCP.2018.19.5.1243 Text en Copyright: © Asian Pacific Journal of Cancer Prevention http://creativecommons.org/licenses/BY-SA/4.0 This work is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License
spellingShingle Research Article
Paramita, P
Wardhani, Bantari WK
Wanandi, Septelia Inawati
Louisa, Melva
Curcumin for the Prevention of Epithelial-Mesenchymal Transition in Endoxifen-Treated MCF-7 Breast Cancer Cells
title Curcumin for the Prevention of Epithelial-Mesenchymal Transition in Endoxifen-Treated MCF-7 Breast Cancer Cells
title_full Curcumin for the Prevention of Epithelial-Mesenchymal Transition in Endoxifen-Treated MCF-7 Breast Cancer Cells
title_fullStr Curcumin for the Prevention of Epithelial-Mesenchymal Transition in Endoxifen-Treated MCF-7 Breast Cancer Cells
title_full_unstemmed Curcumin for the Prevention of Epithelial-Mesenchymal Transition in Endoxifen-Treated MCF-7 Breast Cancer Cells
title_short Curcumin for the Prevention of Epithelial-Mesenchymal Transition in Endoxifen-Treated MCF-7 Breast Cancer Cells
title_sort curcumin for the prevention of epithelial-mesenchymal transition in endoxifen-treated mcf-7 breast cancer cells
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6031844/
https://www.ncbi.nlm.nih.gov/pubmed/29801408
http://dx.doi.org/10.22034/APJCP.2018.19.5.1243
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