phosphatase of regenerating liver 3 (PRL-3) inhibitor
CAS：893449-38-2
分子式：C17H11Br2NO2S2
分子量：485.2
纯度：98%
存储：Store at -20°C

Background:

Phosphatase of regenerating liver 3 (PRL-3; also known as PTP4A3) plays critical roles in cell proliferation, motility, and invasion, and thus contributes to cancer metastasis. PRL-3 inhibitor is a cell-permeable benzylidene rhodamine that inhibits PRL-3 (IC50 = 900 nM for human PRL-3 in vitro), with minimal activity against other phosphatases.[1],[2] It reduces the invasion of mouse melanoma B16F10 cells in a cell-based assay.[1] PRL-3 inhibitor has been used to elucidate the actions of this enzyme, demonstrating that it dephosphorylates Tyr783 on integrin β1 and modulates VEGF-mediated endothelial cell migration.[3],[4] It dose-dependently inhibits the growth and triggers apoptosis in cancer cell lines.[5],[6]

Reference:
[1]. Ahn, J.H., Kim, S.J., Park, W.S., et al. Synthesis and biological evaluation of rhodanine derivatives as PRL-3 inhibitors. Bioorganic & Medicinal Chemistry Letters 16(11), 2996-2999 (2006).
[2]. Min, G., Lee, S.K., Kim, H.N., et al. Rhodanine-based PRL-3 inhibitors blocked the migration and invasion of metastatic cancer cells. Bioorganic & Medicinal Chemistry Letters 23(13), 3769-3774 (2013).
[3]. Tian, W., Qu, L., Meng, L., et al. Phosphatase of regenerating liver-3 directly interacts with integrin β1 and regulates its phosphorylation at tyrosine 783. BMC Biochemistry 13:22, (2012).
[4]. Zimmerman, M.W., McQueeney, K.E., Isenberg, J.S., et al. Protein-tyrosine phosphatase 4A3 (PTP4A3) promotes vascular endothelial growth factor signaling and enables endothelial cell motility. The Journal of Biological Chemisty 289(9), 5904-5913 (2014).
[5]. Ooki, A., Yamashita, K., Kikuchi, S., et al. Therapeutic potential of PRL-3 targeting and clinical significance of PRL-3 genomic amplification in gastric cancer. BMC Cancer 11:122, (2011).
[6]. Zhou, J., Bi, C., Chng, W.J., et al. PRL-3, a metastasis associated tyrosine phosphatase, is involved in FLT3-ITD signaling and implicated in anti-AML therapy. PLoS One 6(5), (2011).