Dickkopf-3 (DKK-3) obstructs VEGFR-2/Akt/mTOR signaling cascade by interacting of 尾2-microglobulin (尾2M) in ovarian tumorigenesis
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- 作者：Boh-Ram Kima ; 1 ; Eun-Ju Leeb ; 1 ; Seung Hee Seoa ; Seung-Hoon Leec ; Seung Bae Rhoa ; sbrho@ncc.re.kr" class="auth_mail" title="E-mail the corresponding author
- 关键词：尾2M ; 尾2-microglobulin ; DKK-3 ; dickkopf-3 ; VEGFR-2 ; vascular endothelial growth factor receptor-2 ; CMV ; cytomegalovirus ; EMT ; epithelial&ndash ; mesenchymal transition ; CREB ; cyclic AMP-responsive element-binding protein ; Dvl ; dishevelled ; siRNA ; small interfering RNA ; ONPG ; o-nitrophenyl 尾-D-galactopyranoside ; CDK ; cyclin-dependent kinases ; mTOR ; mammalian target of rapamycin ; 4E-BP1 ; 4E-binding protein 1
- 刊名：Cellular Signalling
- 出版年：2015
- 出版时间：November 2015
- 年：2015
- 卷：27
- 期：11
- 页码：2150-2159
- 全文大小：1228 K
文摘
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尾2M directly interacts with DKK-3 in biological cellular conditions.
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尾2M recovers DKK-3-induced apoptosis via the inhibition of the VEGFR-2/TSC-2/mTOR signaling.
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尾2M controls the protein level of apoptosis modulators via the reduction of p53 activity.
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DKK-3 suppresses angiogenesis of 尾2M through VEGFR-2 in ovarian tumorigenesis.