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Биологические мембраны: Журнал мембранной и клеточной биологии, 2022, T. 39, № 6, стр. 457-473

Миелоидная дифференцировка повышает устойчивость лейкозных клеток к TRAIL-индуцированной гибели путем снижения экспрессии рецепторов DR4 и DR5

Я. В. Ломовская a, *, М. И. Кобякова a, А. С. Сенотов a, И. С. Фадеева a, b, А. И. Ломовский a, К. С. Краснов a, b, Д. Ю. Штатнова a, b, В. С. Акатов a, b, Р. С. Фадеев a, b

a Институт теоретической и экспериментальной биофизики РАН
142290 Пущино, Московская обл., Россия

b Пущинский государственный естественно-научный институт
142290 Пущино, Московская обл., Россия

* E-mail: yannalomovskaya@gmail.com

Поступила в редакцию 18.04.2022
После доработки 20.06.2022
Принята к публикации 22.06.2022

Аннотация

Изучение механизмов устойчивости опухолевых клеток к TRAIL-индуцированной гибели остается актуальной задачей, так как данный цитокин является важным высокоизбирательным молекулярным эффектором противоопухолевого иммунитета. В нашей работе показано, что у клеток лейкоза человека THP-1, HL-60 и K562 индукция экзогенными факторами миелоидной дифференцировки in vitro во всех направлениях миелопоэза, кроме эритроидоподобного, повышает устойчивость к TRAIL-индуцированной гибели, снижая экспрессию рецепторов DR4 и DR5 на клеточной поверхности. Было установлено также, что ONC201, туникамицин и SAHA (субероиланилид гидроксамовой кислоты), способные вызывать повышение экспрессии DR5 у лейкозных клеток, подавляли их TRAIL-резистентность, индуцированную факторами дифференцировки. Полученные результаты представляют интерес для разработки препаратов и стратегий для повышения эффективности лечения миелоидных лейкозов.

Ключевые слова: лейкозные клетки, цитокин TRAIL, клеточная гибель, миелоидная дифференцировка, резистентность

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