БИОХИМИЯ, 2018, том 83, вып. 12, с. 1779–1790

УДК 616-006.446; 577.29

Роль нарушений сигнального пути WNT в патогенезе лейкозов

Обзор

© 2018 Т.И. Фетисов 1, Е.А. Лесовая 1,2, М.Г. Якубовская 1, К.И. Кирсанов 1,3, Г.А. Белицкий 1*

НМИЦ онкологии им. Н.Н. Блохина Минздрава России, 115478 Москва, Россия; электронная почта: belitsga@mail.ru

Рязанский государственный медицинский университет им. И.П. Павлова, 390026 Рязань, Россия

Российский университет дружбы народов, 117198 Москва, Россия

Поступила в редакцию 01.09.2018

DOI: 10.1134/S0320972518120035

КЛЮЧЕВЫЕ СЛОВА: лейкозы, гемопоэз, сигнальный путь WNT, WNT-лиганды, β-катенин, антагонисты WNT-сигналинга, транскрипционные факторы TCF/Lef.

Аннотация

Сигнальный путь WNT/β-катенин играет важную роль в дифференцировке и пролиферации клеток гемопоэза. В связи с этим в последние годы значительное внимание уделяется изучению роли нарушений передачи WNT-сигнала в патогенезе различных злокачественных новообразований кроветворной системы. Основными механизмами нарушения сигнального пути, выявленными к настоящему времени в лейкозах, являются: повышение чувствительности к WNT-лиганду, эпигенетическая репрессия WNT антагонистов, гиперэкспрессия WNT-лигандов, нарушения деградации β-катенина в цитоплазме и изменение активности TCF/Lef. Соответствующие молекулярные изменения представлены гиперэкспрессией FZD, гиперметилированием промоторов генов SFRP, DKK, WiF, Sox, CXXC, гиперэкспрессией Lef1 и плактоглобина, мутацией GSK3β и фосфорилированием β-катенина киназой BCR-ABL. Систематизации этих данных посвящен представленный обзор.

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Финансирование

Работа выполнена при финансовой поддержке РНФ (проект 17-75-20124).

Конфликт интересов

Авторы заявляют, что у них нет конфликта интересов.

Соблюдение этических норм

Авторы заявляют, что данный обзор литературы не содержит собственных экспериментальных данных, полученных с использованием животных или с участием людей.

Библиографические ссылки на все использованные в обзоре данные других авторов оформлены в соответствии с ГОСТом Р 7 05_2008.

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