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Somatic polyploidy is associated with the upregulation of c-MYC interacting genes and EMT-like signatureстатья
Статья опубликована в высокорейтинговом журнале
Информация о цитировании статьи получена из
Web of Science,
Scopus
Статья опубликована в журнале из списка Web of Science и/или Scopus
Дата последнего поиска статьи во внешних источниках: 5 апреля 2017 г.
- Авторы: Vazquez-Martin Alejandro, Anatskaya Olga V.*., Giuliani Alessandro, Erenpreisa Jekaterina, Huang Sui, Salmina Kristine, Inashkina Inna, Huna Anda, Nikolsky Nikolai N., Vinogradov Alexander E.
- Журнал: Oncotarget
- Том: 7
- Номер: 46
- Год издания: 2016
- Издательство: Impact Journals
- Местоположение издательства: Albany, N.Y., United States
- Первая страница: 75235
- Последняя страница: 75260
- DOI: 10.18632/oncotarget.12118
- Аннотация: *Anatskaya Olga V. - correspondence author, equal contribution with first author. --- The dependence of cancer on overexpressed c-MYC and its predisposition for polyploidy represents a double puzzle. We address this conundrum by crossspecies transcription analysis of c-MYC interacting genes in polyploid vs. diploid tissues and cells, including human vs. mouse heart, mouse vs. human liver and purified 4n vs. 2n mouse decidua cells. Gene-by-gene transcriptome comparison and principal component analysis indicated that c-MYC interactants are significantly overrepresented among ploidy-associated genes. Protein interaction networks and gene module analysis revealed that the most upregulated genes relate to growth, stress response, proliferation, stemness and unicellularity, as well as to the pathways of cancer supported by MAPK and RAS coordinated pathways. A surprising feature was the up-regulation of epithelial-mesenchymal transition (EMT) modules embodied by the N-cadherin pathway and EMT regulators from SNAIL and TWIST families. Metabolic pathway analysis also revealed the EMT-linked features, such as global proteome remodeling, oxidative stress, DNA repair and Warburg-like energy metabolism. Genes associated with apoptosis, immunity, energy demand and tumour suppression were mostly down-regulated. Noteworthy, despite the association between polyploidy and ample features of cancer, polyploidy does not trigger it. Possibly it occurs because normal polyploidy does not go that far in embryonalisation and linked genome destabilisation. In general, the analysis of polyploid transcriptome explained the evolutionary relation of c-MYC and polyploidy to cancer.
- Добавил в систему: Виноградов Александр Евгеньевич