Protein carbonylation as a mechanism of regulation of MCF-7 breast cancer cell proliferation

Tumor progression is accompanied by dysregulation of cell proliferation and apoptosis, which plays an essential role in breast cancer pathogenesis and cell resistance to chemotherapy. The role of protein carbonylation in molecular mechanisms of regulating MCF-7 breast cancer cell proliferation under...

Descripción completa

Guardado en:
Detalles Bibliográficos
Autores principales: E. V. Shakhristova, E. A. Stepovaya, O. L. Nosareva, N. V. Ryazantseva
Formato: article
Lenguaje:RU
Publicado: Scientific Сentre for Family Health and Human Reproduction Problems 2016
Materias:
Q
Acceso en línea:https://doaj.org/article/c4f6e84ab4be4b188250765f7cd94c01
Etiquetas: Agregar Etiqueta
Sin Etiquetas, Sea el primero en etiquetar este registro!
id oai:doaj.org-article:c4f6e84ab4be4b188250765f7cd94c01
record_format dspace
spelling oai:doaj.org-article:c4f6e84ab4be4b188250765f7cd94c012021-11-23T06:14:34ZProtein carbonylation as a mechanism of regulation of MCF-7 breast cancer cell proliferation2541-94202587-959610.12737/article_590823a524b737.92709342https://doaj.org/article/c4f6e84ab4be4b188250765f7cd94c012016-05-01T00:00:00Zhttps://www.actabiomedica.ru/jour/article/view/206https://doaj.org/toc/2541-9420https://doaj.org/toc/2587-9596Tumor progression is accompanied by dysregulation of cell proliferation and apoptosis, which plays an essential role in breast cancer pathogenesis and cell resistance to chemotherapy. The role of protein carbonylation in molecular mechanisms of regulating MCF-7 breast cancer cell proliferation under the effect of roscovitine, a selective inhibitor of cyclin-dependent kinases, was evaluated. The cells were grown in adherent cell culture with or without roscovitine. The levels of reduced/oxidized glutathione and the concentration of protein carbonyl derivatives were determined by spectrophotometry. The cell cycle was evaluated by the flow cytometry; the same technique was used to measure the reactive oxygen species (ROS) concentration. Cell culture with roscovitine resulted in a decrease in the redox potential of the glutathione system and a rise in the ROS and protein carbonyl derivative concentrations. Roscovitine contributed to the G0/G1 and G2/М phase arrest due to its interaction with ATP-binding sites of cyclin-dependent kinases. Roscovitine could also promote enzyme carbonylation. The obtained results can be further used for development of personalized approaches to breast cancer therapy.E. V. ShakhristovaE. A. StepovayaO. L. NosarevaN. V. RyazantsevaScientific Сentre for Family Health and Human Reproduction Problemsarticleprotein carbonyl derivativesproliferationoxidative stressbreast adenocarcinomaScienceQRUActa Biomedica Scientifica, Vol 1, Iss 3(2), Pp 135-137 (2016)
institution DOAJ
collection DOAJ
language RU
topic protein carbonyl derivatives
proliferation
oxidative stress
breast adenocarcinoma
Science
Q
spellingShingle protein carbonyl derivatives
proliferation
oxidative stress
breast adenocarcinoma
Science
Q
E. V. Shakhristova
E. A. Stepovaya
O. L. Nosareva
N. V. Ryazantseva
Protein carbonylation as a mechanism of regulation of MCF-7 breast cancer cell proliferation
description Tumor progression is accompanied by dysregulation of cell proliferation and apoptosis, which plays an essential role in breast cancer pathogenesis and cell resistance to chemotherapy. The role of protein carbonylation in molecular mechanisms of regulating MCF-7 breast cancer cell proliferation under the effect of roscovitine, a selective inhibitor of cyclin-dependent kinases, was evaluated. The cells were grown in adherent cell culture with or without roscovitine. The levels of reduced/oxidized glutathione and the concentration of protein carbonyl derivatives were determined by spectrophotometry. The cell cycle was evaluated by the flow cytometry; the same technique was used to measure the reactive oxygen species (ROS) concentration. Cell culture with roscovitine resulted in a decrease in the redox potential of the glutathione system and a rise in the ROS and protein carbonyl derivative concentrations. Roscovitine contributed to the G0/G1 and G2/М phase arrest due to its interaction with ATP-binding sites of cyclin-dependent kinases. Roscovitine could also promote enzyme carbonylation. The obtained results can be further used for development of personalized approaches to breast cancer therapy.
format article
author E. V. Shakhristova
E. A. Stepovaya
O. L. Nosareva
N. V. Ryazantseva
author_facet E. V. Shakhristova
E. A. Stepovaya
O. L. Nosareva
N. V. Ryazantseva
author_sort E. V. Shakhristova
title Protein carbonylation as a mechanism of regulation of MCF-7 breast cancer cell proliferation
title_short Protein carbonylation as a mechanism of regulation of MCF-7 breast cancer cell proliferation
title_full Protein carbonylation as a mechanism of regulation of MCF-7 breast cancer cell proliferation
title_fullStr Protein carbonylation as a mechanism of regulation of MCF-7 breast cancer cell proliferation
title_full_unstemmed Protein carbonylation as a mechanism of regulation of MCF-7 breast cancer cell proliferation
title_sort protein carbonylation as a mechanism of regulation of mcf-7 breast cancer cell proliferation
publisher Scientific Сentre for Family Health and Human Reproduction Problems
publishDate 2016
url https://doaj.org/article/c4f6e84ab4be4b188250765f7cd94c01
work_keys_str_mv AT evshakhristova proteincarbonylationasamechanismofregulationofmcf7breastcancercellproliferation
AT eastepovaya proteincarbonylationasamechanismofregulationofmcf7breastcancercellproliferation
AT olnosareva proteincarbonylationasamechanismofregulationofmcf7breastcancercellproliferation
AT nvryazantseva proteincarbonylationasamechanismofregulationofmcf7breastcancercellproliferation
_version_ 1718417096240529408