Biphasic activation of extracellular signal-regulated kinase (ERK) 1/2 in epidermal growth factor (EGF)-stimulated SW480 colorectal cancer cells

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Cancer cells have different characteristics due to the genetic differences where these unique features may strongly influence the effectiveness of therapeutic interventions. Here, we show that the spontaneous reactivation of extracellular signal-regulated kinase (ERK), distinct from conventional ERK activation, represents a potent mechanism for cancer cell survival. We studied ERK1/2 activation in vitro in SW480 colorectal cancer cells. Although ERK signaling tends to be transiently activated, we observed the delayed reactivation of ERK1/2 in epidermal growth factor (EGF)-stimulated SW480 cells. This effect was observed even after EGF withdrawal. While phosphorylated ERK1/2 translocated into the nucleus following its primary activation, it remained in the cytoplasm during late-phase activation. The inhibition of primary ERK1/2 activation or protein trafficking, blocked reactivation and concurrently increased caspase 3 activity. Our results suggest that the biphasic activation of ERK1/2 plays a role in cancer cell survival; thus, regulation of ERK1/2 activation may improve the efficacy of cancer therapies that target ERK signaling.
Publisher
KOREAN SOCIETY BIOCHEMISTRY & MOLECULAR BIOLOGY
Issue Date
2016-04
Language
English
Article Type
Article
Keywords

2 DISTINCT PHASES; PROTEIN-KINASE; SUSTAINED ACTIVATION; MAP KINASES; EXPRESSION; PATHWAYS; PROLIFERATION; CASCADE

Citation

BMB REPORTS, v.49, no.4, pp.220 - 225

ISSN
1976-6696
DOI
10.5483/BMBRep.2016.49.4.004
URI
http://hdl.handle.net/10203/212162
Appears in Collection
BiS-Journal Papers(저널논문)
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