Depletion of STYK1 inhibits intrahepatic cholangiocarcinoma development both in vitro and in vivo
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Intrahepatic cholangiocarcinoma (ICC) has been reported to be the second most common primary hepatic carcinoma worldwide, and very limited therapies are currently available. Serine threonine tyrosine kinase (STYK1), a member of the receptor tyrosine kinase family, exhibits tumorigenicity in many types of cancers and is a potential therapeutic target for ICC. In this study, STYK1 was knocked down in the ICC cell lines HCCC-9810 and RBE via a lentivirus-mediated system using short hairpin RNA (shRNA). Next, cell proliferation, colony formation, cell cycle progression, tumor formation in nude mice, migration and invasion, and the expression levels of cell cycle proteins in Lv-sh STYK1- or Lv-sh Con-infected cells were analyzed by CCK-8 assay, colony formation evaluation, flow cytometry, tumor formation evaluation, wound scratch assay, transwell assay, and western blotting. The results indicated that depletion of STYK1 inhibits ICC development both in vitro and in vivo.
KeywordsIntrahepatic cholangiocarcinoma (ICC) STYK1 Biomarker Gene therapy Molecular mechanism
This work was supported by the International Science and Technology Cooperation Program of China (No. 2014DFA31420) and the National Natural Science Foundation of China (No. 81160311).
Compliance with ethical standards
All animal experiments were approved by the Animal Care Committee of the Affiliated Hospital of Guiyang Medical College.
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