Yazarlar |
Hyun-Seok Kim
Türkiye |
Krish Patel
Türkiye |
Kristi Muldoon-Jacobs
Türkiye |
Kheem S Bisht
Türkiye |
Nukhet Aykin-Burns
Türkiye |
J Daniel Pennington
Türkiye |
Der Meer Van
Türkiye |
Phuongmai Nguyen
Türkiye |
Jason Savage
Türkiye |
Kjerstin M Owens
Türkiye |
Athanassios Vassilopoulos
Türkiye |
Özkan ÖZDEN
Kafkas Üniversitesi, Türkiye |
Seong-Hoon Park
Türkiye |
Keshav K Singh
Türkiye |
Abdulkadir Sarki A
Türkiye |
Douglas R Spitz
Türkiye |
Chu-Xia Deng
Türkiye |
David Gius
Türkiye |
Özet |
The sirtuin gene family (SIRT) is hypothesized to regulate the aging process and play a role in cellular repair. This work demonstrates that SIRT3(-/-) mouse embryonic fibroblasts (MEFs) exhibit abnormal mitochondrial physiology as well as increases in stress-induced superoxide levels and genomic instability. Expression of a single oncogene (Myc or Ras) in SIRT3(-/-) MEFs results in in vitro transformation and altered intracellular metabolism. Superoxide dismutase prevents transformation by a single oncogene in SIRT3(-/-) MEFs and reverses the tumor-permissive phenotype as well as stress-induced genomic instability. In addition, SIRT3(-/-) mice develop ER/PR-positive mammary tumors. Finally, human breast and other human cancer specimens exhibit reduced SIRT3 levels. These results identify SIRT3 as a genomically expressed, mitochondria-localized tumor suppressor. |
Anahtar Kelimeler |
Makale Türü | Özgün Makale |
Makale Alt Türü | SSCI, AHCI, SCI, SCI-Exp dergilerinde yayımlanan tam makale |
Dergi Adı | CANCER CELL |
Dergi ISSN | 1535-6108 |
Dergi Tarandığı Indeksler | SCI |
Makale Dili | İngilizce |
Basım Tarihi | 01-2010 |
Cilt No | 17 |
Sayı | 1 |
Sayfalar | 41 / 52 |
Doi Numarası | 10.1016/j.ccr.2009.11.023 |
Makale Linki | http://linkinghub.elsevier.com/retrieve/pii/S1535610809004280 |