Targeting Cadherin-17 Inactivates Wnt Signaling and Inhibits Tumor Growth in Liver Carcinoma
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AbstractHepatocellular carcinoma (HCC) is a lethal malignancy for which there are no effective therapies. To develop rational therapeutic approaches for treating this disease, we are performing proof-of-principle studies targeting molecules crucial for the development of HCC. Here, we show that cadherin-17 (CDH17) adhesion molecule is up-regulated in human liver cancers and can transform premalignant liver progenitor cells to produce liver carcinomas in mice. RNA interference-mediated knockdown of CDH17 inhibited proliferation of both primary and highly metastatic HCC cell lines in vitro and in vivo. The antitumor mechanisms underlying CDH17 inhibition involve inactivation of Wnt signaling, because growth inhibition and cell death were accompanied by relocalization of beta-catenin to the cytoplasm and a concomitant reduction in cyclin D1 and an increase in retinoblastoma. Conclusion: Our results identify CDH17 as a novel oncogene in HCC and suggest that CDH17 is a biomarker and attractive therapeutic target for this aggressive malignancy. (HEPATOLOGY 2009;50:1453-1463.)
All Author(s) ListLiu LX, Lee NP, Chan VW, Xue W, Zender L, Zhang CS, Mao M, Dai HY, Wang XL, Xu MZ, Lee TK, Ng IO, Chen YC, Kung HF, Lowe SW, Poon RTP, Wang JH, Luk JM
Journal nameHepatology
Volume Number50
Issue Number5
PublisherWiley: 12 months
Pages1453 - 1463
LanguagesEnglish-United Kingdom
Web of Science Subject CategoriesGastroenterology & Hepatology; GASTROENTEROLOGY & HEPATOLOGY

Last updated on 2020-18-10 at 01:00