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    Please use this identifier to cite or link to this item: http://ir.nhri.org.tw/handle/3990099045/7444


    Title: CTA095, a novel Etk and Src dual inhibitor, induces apoptosis in prostate cancer cells and overcomes resistance to Src inhibitors
    Authors: Guo, W;Liu, R;Bhardwaj, G;Ma, AH;Changou, C;Yang, JC;Li, Y;Feng, C;Luo, Y;Mazloom, A;Sanchez, E;Wang, Y;Huang, W;Patterson, R;Evans, CP;Lam, KS;Kung, HJ
    Contributors: Institute of Molecular and Genomic Medicine
    Abstract: Etk is a non-receptor tyrosine kinase, which provides a strong survival signal in human prostate cancer cells. Src, another tyrosine kinase that cross-activates with Etk, has been shown to play an important role in prostate cancer metastasis. Herein, we discovered a new class of Etk inhibitors. Within those inhibitors, CTA095 was identified as a potent Etk and Src dual inhibitor. CTA095 was found to induce autophagy as well as apoptosis in human prostate cancer cells. In addition, CTA095 inhibited HUVEC cell tube formation and “wound healing” of human prostate cancer cells, implying its role in inhibition of angiogenesis and metastasis of human prostate cancer. More interestingly, CTA095 could overcome Src inhibitor resistance in prostate cancer cells. It induces apoptosis in Src inhibitor resistant prostate cancer cells, likely through a mechanism of down regulation of Myc and BCL2. This finding indicates that simultaneously targeting Etk and Src could be a promising approach to overcome drug resistance in prostate cancer.
    Date: 2013-08
    Relation: PLoS ONE. 2013 Aug;8(8):Article number e70910.
    Link to: http://dx.doi.org/10.1371/journal.pone.0070910
    JIF/Ranking 2023: http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=NHRI&SrcApp=NHRI_IR&KeyISSN=1932-6203&DestApp=IC2JCR
    Cited Times(WOS): https://www.webofscience.com/wos/woscc/full-record/WOS:000323378000023
    Cited Times(Scopus): http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=84881581558
    Appears in Collections:[龔行健] 期刊論文

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