Rapamycin-induced miR-21 promotes mitochondrial homeostasis and adaptation in mTORC1 activated cells

mTORC1 hyperactivation drives the multi-organ hamartomatous disease tuberous sclerosis complex (TSC). Rapamycin inhibits mTORC1, inducing partial tumor responses; however, the tumors regrow following treatment cessation. We discovered that the oncogenic miRNA, miR-21, is increased in Tsc2-deficient...

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Библиографические подробности
Опубликовано в: :Oncotarget
Главные авторы: Lam, Hilaire C., Liu, Heng-Jia, Baglini, Christian V., Filippakis, Harilaos, Alesi, Nicola, Nijmeh, Julie, Du, Heng, Lope, Alicia Llorente, Cottrill, Katherine A., Handen, Adam, Asara, John M., Kwiatkowski, David J., Ben-Sahra, Issam, Oldham, William M., Chan, Stephen Y., Henske, Elizabeth P.
Формат: Artigo
Язык:Inglês
Опубликовано: Impact Journals LLC 2017
Предметы:
Priority Research Paper
Online-ссылка:https://ncbi.nlm.nih.gov/pmc/articles/PMC5630288/
https://ncbi.nlm.nih.gov/pubmed/29029388
https://ncbi.nlm.nih.govhttp://dx.doi.org/10.18632/oncotarget.19947
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