09-24-2013

Cavin-3 is a tumor suppressor protein of unknown function. Using a combination of in vivo knockout and in vitro gain/loss of function approaches, we show that cavin-3 dictates the balance between ERK and Akt signaling. Loss of cavin-3 increases Akt signaling at the expense of ERK, while gain of cavin-3 increases ERK signaling at the expense Akt. Cavin-3 facilitates signal transduction to ERK by anchoring caveolae, a lipid-raft specialization that contains an ERK activation module, to the membrane skeleton of the plasma membrane. Loss of cavin-3 reduces the number of caveolae, thereby separating this ERK activation module from signaling receptors. Loss of cavin-3 promotes Akt signaling through suppression of EGR1 and PTEN. The in vitro consequences of the loss of cavin-3 include induction of Warburg metabolism (aerobic glycolysis), accelerated cell proliferation and resistance to apoptosis. The in vivo consequences of cavin-3 loss are increased lactate production and cachexia. 9 total samples, consisting of 3 cavin-3 siRNA groups (0 days, 3 days and 8 days) one set was untreated, one set was serum starved, one set was serum starved and then treated with EGF for 1 hr.

not applicable

instance of dataset

E-GEOD-50982

raw

50982

functional genomics

06-03-2014

available

gene expression

Homo sapiens

A-GEOD-10558

Illumina HumanHT-12 V4.0 expression beadchip

ArrayExpress

gzip compressed

TXT

download

none

none

ArrayExpress

gzip compressed

TXT

download

none

none

Gene Expression Omnibus

not compressed

HTML

landing page

true

none

none

EBI

SCR:004727

European Bioinformatics Institute

SCR:002964

ArrayExpress