Title : Rapid activation of ERK1/2 and AKT in human breast cancer cells by cadmium.

Pub. Date : 2008 May 1

PMID : 18275979






7 Functional Relationships(s)
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1 Rapid activation of ERK1/2 and AKT in human breast cancer cells by cadmium. Cadmium mitogen-activated protein kinase 3 Homo sapiens
2 Cadmium (Cd), an endocrine disruptor, can induce a variety of signaling events including the activation of ERK1/2 and AKT. Cadmium mitogen-activated protein kinase 3 Homo sapiens
3 Cadmium (Cd), an endocrine disruptor, can induce a variety of signaling events including the activation of ERK1/2 and AKT. Cadmium mitogen-activated protein kinase 3 Homo sapiens
4 Specifically, treatment of MCF-7 cells, that express ER alpha, ER beta and GPR30, to 0.5-10 microM Cd for only 2.5 min resulted in transient phosphorylation of ERK1/2. Cadmium mitogen-activated protein kinase 3 Homo sapiens
5 In SK-BR-3 cells, that express only GPR30, Cd also caused a transient activation of ERK1/2, but not of AKT. Cadmium mitogen-activated protein kinase 3 Homo sapiens
6 While the estrogen receptor antagonist, ICI 182,780, did not prevent the effect of Cd on these signals, specific siRNA against hER alpha significantly reduced Cd-induced activation of ERK1/2 and completely blocked the activation of AKT. Cadmium mitogen-activated protein kinase 3 Homo sapiens
7 It is concluded that Cd, like estradiol, can cause rapid activation of ERK1/2 and AKT and that these signaling events are mediated by possible interaction with membrane ER alpha and GPR30, but not ER beta. Cadmium mitogen-activated protein kinase 3 Homo sapiens