{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,20]],"date-time":"2026-09-20T23:22:42Z","timestamp":1789946562976,"version":"4.0.1"},"reference-count":47,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2018,10,26]],"date-time":"2018-10-26T00:00:00Z","timestamp":1540512000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["J of Cellular Biochemistry"],"published-print":{"date-parts":[[2019,4]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:sec><jats:title>Background<\/jats:title><jats:p>The objective of this study was to clarify the molecular pathways involved in hepatitis B virus (HBV)\u2010induced hepatoblastoma.<\/jats:p><\/jats:sec><jats:sec><jats:title>Method<\/jats:title><jats:p>The expression of factors in different signaling pathways (H19, miR\u2010675, miR\u2010138, protein tyrosine kinase 2 [PTK2], fas\u2010associated death domain [FADD], hypoxia\u2010inducible factor 1\u2010alpha [HIFIA], focal adhesion kinase [FAK], caspase\u20108, and caspase\u20103) was compared between HBV (+) and HBV (\u2212) groups using quantitative real\u2010time polymerase chain reaction and Western blot analysis. Subsequently, immunohistochemistry (IHC) and TdT\u2010mediated dUTP Nick\u2010End Labeling (TUNEL) assays were used to verify the expression of above proteins in HBV (+) and HBV (\u2212) groups. Computational analysis was conducted to predict the target genes of miR\u2010675 and miR\u2010138, whose regulatory relationships were then clarified using luciferase assays and cell transfection studies.<\/jats:p><\/jats:sec><jats:sec><jats:title>Result<\/jats:title><jats:p>The expression of H19, miR\u2010675, PTK2, HIFIA, and FAK was increased in the HBV (+) group, while the expression of miR\u2010138, FADD, caspase\u20108, and caspase\u20103 was decreased in the HBV (+) group. FADD and PTK2 were identified as target genes of miR\u2010675 and miR\u2010138, respectively. In addition, miR\u2010675 was upregulated while miR\u2010138 was downregulated by X protein (HBx).<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion<\/jats:title><jats:p>In summary, the results of this study revealed the molecular pathways involved in HBV\u2010induced hepatoblastoma. In the presence of HBV, HBX upregulated the expression of H19 through HIFIA. Consecutively, overexpressed H19 upregulated the expression of PTK2 via targeting miR\u2010138 and downregulated the expression of FADD via targeting miR\u2010675. Finally, increased expression of PTK2 and reduced expression of FADD both led to the inhibition of cell apoptosis, thus promoting the tumorigenesis of hepatoblastoma.<\/jats:p><\/jats:sec>","DOI":"10.1002\/jcb.27797","type":"journal-article","created":{"date-parts":[[2018,10,27]],"date-time":"2018-10-27T05:04:00Z","timestamp":1540616640000},"page":"5218-5231","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":16,"title":["RETRACTED: H19 suppresses the growth of hepatoblastoma cells by promoting their apoptosis via the signaling pathways of miR\u2010675\/FADD and miR\u2010138\/PTK2"],"prefix":"10.1002","volume":"120","author":[{"given":"Lili","family":"Ge","sequence":"first","affiliation":[{"name":"Henan Provincial Key Laboratory of Children\u2019s Genetics and Metabolic Diseases Children\u2019s Hospital Affiliated to Zhengzhou University (Henan Children\u2019s Hospital, Zhengzhou Children\u2019s Hospital) Zhengzhou Henan 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