SETDB1 fuels the lung cancer phenotype by modulating epigenome, 3D genome organization and chromatin mechanical properties

Zakharova, V.V.; Magnitov, M.D.; Del Maestro, L.; Ulianov, S.V.; Glentis, A.; Uyanik, B.; Williart, A.; Karpukhina, A.; Demidov, O.; Joliot, V.; Vassetzky, Y.S.; Mège, R.; Piel, M.; Razin, S.V.; Ait-Si-Ali, S.

Авторы: Zakharova Vlada V., Magnitov Mikhail D., Del Maestro Laurence, Ulianov Sergey V., Glentis Alexandros, Uyanik Burhan, Williart Alice, Karpukhina Anna, Demidov Oleg, Joliot Veronique, Vassetzky Yegor S., Mège René-Marc, Piel Matthieu, Razin Sergey V., Ait-Si-Ali Slimane
Журнал: Nucleic Acids Research
Год издания: 2022
Издательство: Oxford University Press
Местоположение издательства: United Kingdom
Первая страница: 1
Последняя страница: 25
Номер статьи: gkac234
DOI: 10.1093/nar/gkac234
Аннотация: Imbalance in the finely orchestrated system of chromatin-modifying enzymes is a hallmark of many pathologies such as cancers, since causing the affection of the epigenome and transcriptional reprogramming. Here, we demonstrate that a loss-of-function mutation (LOF) of the major histone lysine methyltransferase SETDB1 possessing oncogenic activity in lung cancer cells leads to broad changes in the overall architecture and mechanical properties of the nucleus through genome-wide redistribution of heterochromatin, which perturbs chromatin spatial compartmentalization. Together with the enforced activation of the epithelial expression program, cytoskeleton remodeling, reduced proliferation rate and restricted cellular migration, this leads to the reversed oncogenic potential of lung adenocarcinoma cells. These results emphasize an essential role of chromatin architecture in the determination of oncogenic programs and illustrate a relationship between gene expression, epigenome, 3D genome and nuclear mechanics.
Добавил в систему: Ульянов Сергей Владимирович

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SETDB1 fuels the lung cancer phenotype by modulating epigenome, 3D genome organization and chromatin mechanical propertiesстатья

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