Differential response to α-oxoaldehydes in tamoxifen resistant MCF-7 breast cancer cells.

Tamoxifen is the standard adjuvant endocrine therapy for estrogen-receptor positive premenopausal breast cancer patients. However, tamoxifen resistance is frequently observed under therapy. A tamoxifen resistant cell line has been generated from the estrogen receptor positive mamma carcinoma cell li...

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Autores principales:	Norbert Nass, Hans-Jürgen Brömme, Roland Hartig, Sevil Korkmaz, Saadettin Sel, Frank Hirche, Aoife Ward, Andreas Simm, Stefan Wiemann, Anne E Lykkesfeldt, Albert Roessner, Thomas Kalinski
Formato:	article
Lenguaje:	EN
Publicado:	Public Library of Science (PLoS) 2014
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/ed2045353b0b4f2a9dcd740c593f972e
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spelling	oai:doaj.org-article:ed2045353b0b4f2a9dcd740c593f972e2021-11-25T06:10:13ZDifferential response to α-oxoaldehydes in tamoxifen resistant MCF-7 breast cancer cells.1932-620310.1371/journal.pone.0101473https://doaj.org/article/ed2045353b0b4f2a9dcd740c593f972e2014-01-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/24983248/pdf/?tool=EBIhttps://doaj.org/toc/1932-6203Tamoxifen is the standard adjuvant endocrine therapy for estrogen-receptor positive premenopausal breast cancer patients. However, tamoxifen resistance is frequently observed under therapy. A tamoxifen resistant cell line has been generated from the estrogen receptor positive mamma carcinoma cell line MCF-7 and was analyzed for putative differences in the aldehyde defence system and accumulation of advanced glycation end products (AGE). In comparison to wt MCF-7 cells, these tamoxifen resistant cells were more sensitive to the dicarbonyl compounds glyoxal and methylglyoxal and displayed increased caspase activity, p38-MAPK- and IκBα-phosphorylation. However, mRNA accumulation of the aldehyde- and AGE-defence enzymes glyoxalase-1 and -2 (GLO1, GLO2) as well as fructosamine-3-kinase (FN3K) was not significantly altered. Tamoxifen resistant cells contained less free sulfhydryl-groups (glutathione) suggesting that the increased sensitivity towards the dicarbonyls was due to a higher sensitivity towards reactive oxygen species which are associated with dicarbonyl stress. To further analyse, if these data are of more general importance, key experiments were replicated with tamoxifen resistant MCF-7 cell lines from two independent sources. These cell lines were also more sensitive to aldehydes, especially glyoxal, but were different in their cellular signalling responses to the aldehydes. In conclusion, glyoxalases and other aldehyde defence enzymes might represent a promising target for the therapy of tamoxifen resistant breast cancers.Norbert NassHans-Jürgen BrömmeRoland HartigSevil KorkmazSaadettin SelFrank HircheAoife WardAndreas SimmStefan WiemannAnne E LykkesfeldtAlbert RoessnerThomas KalinskiPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 9, Iss 7, p e101473 (2014)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Norbert Nass Hans-Jürgen Brömme Roland Hartig Sevil Korkmaz Saadettin Sel Frank Hirche Aoife Ward Andreas Simm Stefan Wiemann Anne E Lykkesfeldt Albert Roessner Thomas Kalinski Differential response to α-oxoaldehydes in tamoxifen resistant MCF-7 breast cancer cells.
description	Tamoxifen is the standard adjuvant endocrine therapy for estrogen-receptor positive premenopausal breast cancer patients. However, tamoxifen resistance is frequently observed under therapy. A tamoxifen resistant cell line has been generated from the estrogen receptor positive mamma carcinoma cell line MCF-7 and was analyzed for putative differences in the aldehyde defence system and accumulation of advanced glycation end products (AGE). In comparison to wt MCF-7 cells, these tamoxifen resistant cells were more sensitive to the dicarbonyl compounds glyoxal and methylglyoxal and displayed increased caspase activity, p38-MAPK- and IκBα-phosphorylation. However, mRNA accumulation of the aldehyde- and AGE-defence enzymes glyoxalase-1 and -2 (GLO1, GLO2) as well as fructosamine-3-kinase (FN3K) was not significantly altered. Tamoxifen resistant cells contained less free sulfhydryl-groups (glutathione) suggesting that the increased sensitivity towards the dicarbonyls was due to a higher sensitivity towards reactive oxygen species which are associated with dicarbonyl stress. To further analyse, if these data are of more general importance, key experiments were replicated with tamoxifen resistant MCF-7 cell lines from two independent sources. These cell lines were also more sensitive to aldehydes, especially glyoxal, but were different in their cellular signalling responses to the aldehydes. In conclusion, glyoxalases and other aldehyde defence enzymes might represent a promising target for the therapy of tamoxifen resistant breast cancers.
format	article
author	Norbert Nass Hans-Jürgen Brömme Roland Hartig Sevil Korkmaz Saadettin Sel Frank Hirche Aoife Ward Andreas Simm Stefan Wiemann Anne E Lykkesfeldt Albert Roessner Thomas Kalinski
author_facet	Norbert Nass Hans-Jürgen Brömme Roland Hartig Sevil Korkmaz Saadettin Sel Frank Hirche Aoife Ward Andreas Simm Stefan Wiemann Anne E Lykkesfeldt Albert Roessner Thomas Kalinski
author_sort	Norbert Nass
title	Differential response to α-oxoaldehydes in tamoxifen resistant MCF-7 breast cancer cells.
title_short	Differential response to α-oxoaldehydes in tamoxifen resistant MCF-7 breast cancer cells.
title_full	Differential response to α-oxoaldehydes in tamoxifen resistant MCF-7 breast cancer cells.
title_fullStr	Differential response to α-oxoaldehydes in tamoxifen resistant MCF-7 breast cancer cells.
title_full_unstemmed	Differential response to α-oxoaldehydes in tamoxifen resistant MCF-7 breast cancer cells.
title_sort	differential response to α-oxoaldehydes in tamoxifen resistant mcf-7 breast cancer cells.
publisher	Public Library of Science (PLoS)
publishDate	2014
url	https://doaj.org/article/ed2045353b0b4f2a9dcd740c593f972e
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Differential response to α-oxoaldehydes in tamoxifen resistant MCF-7 breast cancer cells.

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