Apoptosis induced by PGC-1β in breast cancer cells is mediated by the mTOR pathway.

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 Rep

journal_title

Oncology reports

authors

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 H

doi

10.3892/or.2013.2628

subject

Has Abstract

pub_date

2013-10-01 00:00:00

pages

1631-8

issue

4

eissn

1021-335X

issn

1791-2431

journal_volume

30

pub_type

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