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Keywords {🔍}

cwp, cancer, cells, prostate, pubmed, article, cell, βcatenin, google, scholar, wntβcatenin, stress, cas, signaling, lncap, fig, pathway, crpc, protein, wnt, control, exposed, apoptosis, activity, central, growth, assay, induces, study, results, western, expression, analysis, data, endoplasmic, reticulum, androgen, patients, treatment, tumor, performed, mice, stem, inhibitor, lee, viability, forward, reverse, means, castrationresistant,

Topics {✒️}

compound z-valine-alanine-aspartate-fluoromethylketone alters cbp/β-catenin-dependent transcription cell-permeable pan-caspase inhibitor wnt/β-catenin pathway modulators inhibit wnt/β-catenin signaling wnt/β-catenin signaling cascade interferon-α/5-fluorouracil combination therapy wnt/β-catenin signaling pathway wnt/β-catenin signaling modulation wnt/β-catenin inhibitor cwp232291 wnt/β-catenin signaling plays targeting wnt/β-catenin signaling β-catenin-dependent canonical pathway castration-resistant prostate cancer chan-hee park wnt/β-catenin inhibitor castrate-resistant prostate cancer tcf/lef reporter construct jung-hyuck park lef/tcf family members article download pdf wnt/β-catenin pathway wnt/β-catenin pathway [17] wnt/β-catenin signaling beta-catenin/apc pathway hormone-naïve prostate cancer er stress-related markers endoplasmic reticulum stress peptidomimetic small molecule lef/tcf reporter activity wnt/β-catenin inhibition tcf/lef-binding sites β-catenin-dependent transcription [7 metastatic prostate cancer endoplasmic reticulum chaperones article pak induces tumor-selective apoptosis concentration-time profile indicating potent growth-inhibiting optimem® reduced-serum medium favorable safety profile abrogated cwp232291-induced apoptosis cell-free medium wnt signaling pathway wnt pathway modulation kyoung-june lee full access cyclooxygenase-2-independent anticarcinogenic effects central organelle involved cwp232291-treated cell lines

Questions {❓}

• Targeting Wnt signaling: can we safely eradicate cancer stem cells?

Schema {🗺️}

WebPage:
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         headline:The small molecule WNT/β-catenin inhibitor CWP232291 blocks the growth of castration-resistant prostate cancer by activating the endoplasmic reticulum stress pathway
         description:Androgen receptor (AR)-targeted treatments improve the survival of castration-resistant prostate cancer (CRPC) patients; however, secondary resistance to these agents ultimately occurs in virtually all patients. Therefore, alternative therapeutic targets are urgently needed. Since growing evidence demonstrates that WNT/β-catenin signaling plays an important role in CRPC, the antitumor activity and mechanism of action of CWP232291, a small molecule β-catenin inhibitor, were investigated in prostate cancer. We assessed the antitumor activity of CWP232291 in prostate cancer cell lines and primary cells derived from CRPC patients. The effect of CWP232291 on apoptotic cell death, endoplasmic reticulum (ER) stress, cell viability, and WNT/β-catenin signaling was evaluated by flow cytometry, western blotting, luciferase reporter assay, and fluorescence microscopy. Antitumor efficacy was assessed in two CRPC xenograft mouse models. CWP232291 induced ER stress, resulting in upregulation of the proapoptotic protein CHOP and activation of caspase-3-dependent apoptosis. In addition, CWP232291 suppressed the expression of β-catenin by affecting WNT-dependent transcriptional activity, and downregulated AR and its splice variants in prostate cancer cells. Antitumor activity was observed in prostate cancer cells in vitro and ex vivo, and antitumor efficacy was observed in vivo. Beyond providing preclinical evidence of therapeutic efficacy for the novel small molecule β-catenin inhibitor CWP232291 in CRPC, our results show that inducing ER stress and targeting WNT/β-catenin signaling may be a novel strategy against CRPC.
         datePublished:2019-08-06T00:00:00Z
         dateModified:2019-10-31T00:00:00Z
         pageStart:1
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         keywords:
            Prostate cancer
            Castration-resistant
            WNT signaling pathway
            Endoplasmic reticulum stress
            Cancer Research
            Immunology
            Apoptosis
            Oncology
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      headline:The small molecule WNT/β-catenin inhibitor CWP232291 blocks the growth of castration-resistant prostate cancer by activating the endoplasmic reticulum stress pathway
      description:Androgen receptor (AR)-targeted treatments improve the survival of castration-resistant prostate cancer (CRPC) patients; however, secondary resistance to these agents ultimately occurs in virtually all patients. Therefore, alternative therapeutic targets are urgently needed. Since growing evidence demonstrates that WNT/β-catenin signaling plays an important role in CRPC, the antitumor activity and mechanism of action of CWP232291, a small molecule β-catenin inhibitor, were investigated in prostate cancer. We assessed the antitumor activity of CWP232291 in prostate cancer cell lines and primary cells derived from CRPC patients. The effect of CWP232291 on apoptotic cell death, endoplasmic reticulum (ER) stress, cell viability, and WNT/β-catenin signaling was evaluated by flow cytometry, western blotting, luciferase reporter assay, and fluorescence microscopy. Antitumor efficacy was assessed in two CRPC xenograft mouse models. CWP232291 induced ER stress, resulting in upregulation of the proapoptotic protein CHOP and activation of caspase-3-dependent apoptosis. In addition, CWP232291 suppressed the expression of β-catenin by affecting WNT-dependent transcriptional activity, and downregulated AR and its splice variants in prostate cancer cells. Antitumor activity was observed in prostate cancer cells in vitro and ex vivo, and antitumor efficacy was observed in vivo. Beyond providing preclinical evidence of therapeutic efficacy for the novel small molecule β-catenin inhibitor CWP232291 in CRPC, our results show that inducing ER stress and targeting WNT/β-catenin signaling may be a novel strategy against CRPC.
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      dateModified:2019-10-31T00:00:00Z
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      sameAs:https://doi.org/10.1186/s13046-019-1342-5
      keywords:
         Prostate cancer
         Castration-resistant
         WNT signaling pathway
         Endoplasmic reticulum stress
         Cancer Research
         Immunology
         Apoptosis
         Oncology
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            address:
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               type:PostalAddress
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            address:
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            type:Organization
      name:Hanjong Ahn
      affiliation:
            name:University of Ulsan College of Medicine, Asan Medical Center
            address:
               name:Department of Urology, University of Ulsan College of Medicine, Asan Medical Center, Seoul, South Korea
               type:PostalAddress
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      email:[email protected]
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      name:Department of Urology, Center for Urologic Cancer, National Cancer Center, Goyang, South Korea
      name:Department of Urology, University of Ulsan College of Medicine, Ulsan University Hospital, Ulsan, South Korea
      name:Department of Urology, University of Ulsan College of Medicine, Asan Medical Center, Seoul, South Korea
      name:Asan Institute for Life Science, Asan Medical Center, Seoul, South Korea
      name:Drug Discovery Center, JW Pharmaceutical Corporation, Seoul, South Korea
      name:Drug Discovery Center, JW Pharmaceutical Corporation, Seoul, South Korea
      name:JW Creagene Corporation, Seongnam, South Korea
      name:Department of Urology, University of Ulsan College of Medicine, Asan Medical Center, Seoul, South Korea
      name:Department of Urology, University of Ulsan College of Medicine, Asan Medical Center, Seoul, South Korea

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