Abstract:
:The peroxisome proliferator-activated receptor-γ (PPAR-γ) coactivator-1β (PGC-1β) is a well-established regulator of mitochondrial biogenesis. However, the underlying mechanism of PGC-1β action remains elusive. This study reveals that knockdown of endogenous PGC-1β by short-hairpin RNA (shRNA) leads to a decrease in the expression of mammalian target of rapamycin (mTOR) pathway-related genes in MDA-MB-231 cells. After knockdown of PGC-1β, phosphorylation of AMP-activated protein kinase (AMPK), phosphorylation of Rictor on Thr1135, Raptor and S6 protein was inhibited. However, Akt phosphorylation on Ser473 was upregulated and cell apoptosis occurred. In particular, we demonstrate that the levels of PGC-1β and mTOR correlated with overall mitochondrial activity. These results provide new evidence that cell apoptosis is orchestrated by the balance between several signaling pathways, and that PGC-1β takes part in these events in breast cancer cells mediated by the mTOR signaling pathway.
journal_name
Oncol Repjournal_title
Oncology reportsauthors
Wang L,Liu Q,Li F,Qiu J,Fan H,Ma H,Zhu Y,Wu L,Han X,Yang Z,Jiang H,Wei J,Xia Hdoi
10.3892/or.2013.2628subject
Has Abstractpub_date
2013-10-01 00:00:00pages
1631-8issue
4eissn
1021-335Xissn
1791-2431journal_volume
30pub_type
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