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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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| Опубликовано в: : | Oncotarget |
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| Главные авторы: | , , , , , , , , , , , , , , , |
| Формат: | Artigo |
| Язык: | Inglês |
| Опубликовано: |
Impact Journals LLC
2017
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| Предметы: | |
| 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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