Влияние ожирения на развитие и прогрессию злокачественных новообразований: обзор современных данных и новых терапевтических мишеней
Автор: Семина Е.В., Данилова Н.В., Олейникова Н.А., Агапов М.А., Рубина К.А.
Журнал: Сибирский онкологический журнал @siboncoj
Рубрика: Обзоры
Статья в выпуске: 4 т.20, 2021 года.
Бесплатный доступ
Актуальность. Известно, что диабет 2-го типа, синдром обструктивного апноэ сна, остеоартроз и ряд злокачественных новообразований коррелируют с ожирением. Механизмы, обусловливающие взаимосвязь метаболических нарушений с возникновением злокачественных опухолей, пока неизвестны; значительную роль может играть изменение чувствительности к инсулину и факторам роста, изменение спектра секретируемых адипокинов или особенности их взаимодействия с рецепторами, изменение содержания стероидных половых гормонов в организме, а также особенности метаболизма глюкозы в опухолевых клетках (так называемый эффект Варбурга). Материал и методы. Проведен поиск источников, включая научные, клинические и обзорные статьи, опубликованные в рецензируемых журналах, индексируемых в pubmed, Wos, scopus и РИНЦ. Проанализировано более 150 статей, посвященных изучению взаимосвязи метаболических нарушений с опухолевой прогрессией, из которых 69 включены в данный обзор. Результаты. Основная стратегия лечения опухолевых заболеваний заключается в подавлении пролиферации опухолевых клеток и процессов метастазирования. Возможно, что значительную роль в этих процессах играет ряд факторов, способных усиливать побочные эффекты противоопухолевой терапии, поддерживать резистентность опухолевых клеток или изменять их метаболический профиль. Имеются новые данные о функции таких белков, как Т-кадгерин и рецептор урокиназы (upaR), и их возможном участии в регуляции метаболизма опухолевых клеток, в частности чувствительности к инсулину и гормонам жировой ткани. Помимо адипокинов как уже известных посредников, участвующих в канцерогенезе, в обзоре описаны новые данные о роли Т-кадгерина и урокиназного рецептора upaR в регуляции обменных процессов. Предложена модель, объясняющая взаимосвязь этих белков и метаболических нарушений, ассоциированных с процессами канцерогенеза и химиорезистентности опухолевых клеток. Заключение. Понимание факторов и механизмов, поддерживающих ожирение и нарушения метаболизма, с точки зрения их роли в канцерогенезе актуально как для разработки профилактических мер, так и для оптимизации терапевтических стратегий борьбы с опухолевыми заболеваниями.
Метаболический синдром, ожирение, инсулин, инсулинорезистентность, адипонектин, Т-кадгерин, рецептор урокиназы
Короткий адрес: https://sciup.org/140254543
IDR: 140254543 | DOI: 10.21294/1814-4861-2021-20-4-130-145
Список литературы Влияние ожирения на развитие и прогрессию злокачественных новообразований: обзор современных данных и новых терапевтических мишеней
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