IWP-2 - CAS 686770-61-6
Catalog number: B0084-272158
Category: Inhibitor
Not Intended for Therapeutic Use. For research use only.
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B0084-272158 50 mg $198 In stock
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1.The Wnt signalling pathway is upregulated in an in vitro model of acquired tamoxifen resistant breast cancer.
Loh YN1, Hedditch EL, Baker LA, Jary E, Ward RL, Ford CE. BMC Cancer. 2013 Apr 2;13:174. doi: 10.1186/1471-2407-13-174.
BACKGROUND: Acquired resistance to Tamoxifen remains a critical problem in breast cancer patient treatment, yet the underlying causes of resistance have not been fully elucidated. Abberations in the Wnt signalling pathway have been linked to many human cancers, including breast cancer, and appear to be associated with more metastatic and aggressive types of cancer. Here, our aim was to investigate if this key pathway was involved in acquired Tamoxifen resistance, and could be targeted therapeutically.
2.[Regulating effect of anodonta glucan HBP-A on chondrocytes through Wnt pathway].
Wei SP, Ding DF, Wang XZ, Pang J, Zheng YX, Xu QG, Cao YL, Zhan HS. Zhongguo Gu Shang. 2014 Jun;27(6):461-5.
OBJECTIVE: To investigate regulation function of anodonta glucan HBP-A on chondrocytes through Wnt pathway in vitro.
3.Wnt/Glycogen Synthase Kinase 3β/β-catenin Signaling Activation Mediated Sevoflurane Preconditioning-induced Cardioprotection.
Liu JD1, Deng Q, Tian HH, Pang YT, Deng GL. Chin Med J (Engl). 2015 Sep 5;128(17):2346-53. doi: 10.4103/0366-6999.163375.
BACKGROUND: Sevoflurane preconditioning (SP) has been shown to invoke potent myocardial protection in animal studies and clinical trials. However, the mechanisms underlying SP are complex and not yet well understood. We investigated the hypothesis that the cardioprotection afforded by SP is mediated via the Wnt/glycogen synthase kinase 3β (GSK3β)/β-catenin signaling pathway.
4.ERG is a critical regulator of Wnt/LEF1 signaling in prostate cancer.
Wu L1, Zhao JC, Kim J, Jin HJ, Wang CY, Yu J. Cancer Res. 2013 Oct 1;73(19):6068-79. doi: 10.1158/0008-5472.CAN-13-0882. Epub 2013 Aug 1.
Chromosomal translocations juxtaposing the androgen-responsive TMPRSS2 promoter with the ETS-family transcription factor ERG result in aberrant ERG upregulation in approximately 50% of prostate cancers. Studies to date have shown important roles of ERG in inducing oncogenic properties of prostate cancer. Its molecular mechanisms of action, however, are yet to be fully understood. Here, we report that ERG activates Wnt/LEF1 signaling cascade through multiple mechanisms. ERG bound to the promoters of various Wnt genes to directly increase ligand expression. Consequently, ERG overexpression increased active β-catenin level in the cells and enhanced TCF/LEF1 luciferase reporter activity, which could be partially blocked by WNT-3A inhibitor IWP-2. Most importantly, our data defined LEF1 as a direct target of ERG and that LEF1 inhibition fully abolished ERG-induced Wnt signaling and target gene expression. Furthermore, functional assays showed that Wnt/LEF1 activation phenocopied that of ERG in inducing cell growth, epithelial-to-mesenchymal transition, and cell invasion, whereas blockade of Wnt signaling attenuated these effects.
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