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Beta catenin is degraded by both caspase-3 and proteasomal activity during resveratrol-induced apoptosis in HeLa cells in a GSK3β-independent manner

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Title Beta catenin is degraded by both caspase-3 and proteasomal activity during resveratrol-induced apoptosis in HeLa cells in a GSK3β-independent manner
 
Creator Ray, Mahan
Rai, Neha
Jana, Kuladip
Ghatak, Supratim
Basu, Arnab
Mustafi, Soumyajit Banerjee
Raha, Sanghamitra
 
Subject Resveratrol
HeLa
Apoptosis
β-Catenin
Caspase-3
GSK3β
Proteasomal degradation
 
Description 7-13
Increased activity of β-catenin, an important
transcriptional activator for survival and proliferation-associated
genes has been linked with many cancers. We examined whether β-catenin is a
target of resveratrol and whether
its degradation contributes to the pro-apoptotic effects of resveratrol. HeLa
cells were exposed to 60 µM resveratrol
for 48 h. Apoptosis was confirmed by measurement of annexin V externalization,
caspase-3 activation and
DNA fragmentation. Induction of apoptosis was observed as early as 12 h, when
both caspase-3 activation and PARP (poly ADP ribose polymerase) cleavage
occurred. Nuclear β-catenin levels remained unchanged for 48 h during
resveratrol exposure. However, extranuclear cell lysate β-catenin underwent a
decrease at a late stage of apoptosis namely at 36-48 h. Alterations in the
phosphorylation status of Akt/GSK3β were not observed during
resveratrol-induced apoptosis. Furthermore, inhibition of GSK3β activity which
is largely responsible for β-catenin degradation failed
to influence β-catenin stability. However, inhibition of caspase-3 activity
prevented the decline in β-catenin levels at
36-48 h of resveratrol exposure. Lactacystin, a proteosomal inhibitor also
prevented the degradation of β-catenin
by resveratrol. In conclusion, resveratrol induced apoptosis in HeLa cells in
an Akt/GSK3β-independent manner and down-regulated β-catenin levels during
apoptosis through action of caspase-3 and proteasomal degradation, independent
of GSK3β-mediated phosphorylation.
 
Date 2015-03-30T04:36:47Z
2015-03-30T04:36:47Z
2015-02
 
Type Article
 
Identifier 0975-0959 (Online); 0301-1208 (Print)
http://hdl.handle.net/123456789/31258
 
Language en_US
 
Rights CC Attribution-Noncommercial-No Derivative Works 2.5 India
 
Publisher NISCAIR-CSIR, India
 
Source IJBB Vol.52(1) [February 2015]