Выберите категорию обращения:
Общие вопросы
Отчеты
Рейтинги
Мониторинговый отчёт
Диссертационные советы
Конкурсы
Ввод данных
Структура организаций
Аспирантура
Научное оборудование
Импорт педагогической нагрузки
Журналы и импакт-факторы
Тема обращения:
Описание проблемы:
Введите почтовый адрес:
ИСТИНА
Войти в систему
Регистрация
ИПМех РАН
Главная
Поиск
Статистика
О проекте
Помощь
Ras-induced ROS upregulation affecting cell proliferation is connected with cell type-specific alterations of HSF1/SESN3/p21Cip1/WAF1 pathways
статья
Статья опубликована в высокорейтинговом журнале
Статья опубликована в журнале из списка Web of Science и/или Scopus
Авторы:
Zamkova M.
,
Khromova N.
,
Kopnin B.P.
,
Kopnin P.
Журнал:
Cell Cycle
Том:
12
Номер:
5
Год издания:
2013
Издательство:
Landes Bioscience
Местоположение издательства:
United States
Первая страница:
826
Последняя страница:
836
DOI:
10.4161/cc.23723
Аннотация:
Oncogenes of the RAS family regulate many of the cell’s activities, including proliferation, survival and differentiation. Activating mutations in these genes are common events for many types of cancer. One of the contradictory points concerning the biological significance of Ras activation is its dual effect (pro- or anti-proliferative) on cell reproduction. One of mechanisms by which Ras proteins influence cell growth is a regulation of intracellular level of reactive oxygen species (ROS), second messengers affecting variety of cellular processes including cell proliferation. Recently it was shown that repression of SESN1 and SESN3 genes, whose protein products control regeneration of peroxiredoxins, can play a critical role in Ras-induced ROS upregulation. In the present study we have found that Ras-induced repression of SESN3 expression and ROS upregulation is mediated via the modifications of transcriptional activity of HSF1. Interestingly, mutant Ras overexpression altered the activity of HSF1 in opposite directions in different cell contexts, in particular in human normal fibroblasts and HaCaT immortalized keratinocytes, but these opposite changes caused similar repression of SESN3 expression followed by elevation of ROS content and inhibition of cell proliferation in corresponding cell types. The inhibitory effect on cell proliferation was mediated by upregulation of p21Cip1/WAF1. Thus, HSF1/SESN3/ROS/p21 Cip1/WAF1- mediated deceleration of cell growth may contribute to cell defense systems protecting the organism from excessive proliferation of cells that overexpress activated Ras oncoproteins. Copyright © 2013 Landes Bioscience.
Добавил в систему:
Замкова Мария Анатольевна