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All rights reserved. http://resource.belframework.org/belframework/1.0/knowledge/large_corpus.bel http://purl.org/dc/elements/1.1/title BEL Framework Large Corpus Document http://resource.belframework.org/belframework/1.0/knowledge/large_corpus.bel http://purl.org/pav/authoredBy http://www.tkuhn.ch/bel2nanopub/RAngYnlHdyJCjKthysybi1seO-xLnb_AytvXzhhfRGOlo#_6 http://resource.belframework.org/belframework/1.0/knowledge/large_corpus.bel http://purl.org/pav/version 1.4 http://www.tkuhn.ch/bel2nanopub/RAngYnlHdyJCjKthysybi1seO-xLnb_AytvXzhhfRGOlo#_5 http://www.w3.org/ns/prov#value The PTEN gene (phosphatase and tensin homologous on chromosome 10) is frequently mutated or deleted in a number of malignancies including human hepatocellular carcinoma (HCC). We reported previously that the hepatitis B virus X (HBx) protein, known to be a causative agent in the formation of HCC, activates insulin-like growth factor II (IGF-II) expression through Sp1 phosphorylation by protein kinase C (PKC) or mitogen-activated protein kinase (MAPK) signaling. In this report we demonstrate that the PTEN effect on HBx induced IGF-II activation in a hepatoma cell line. Expression of PTEN and IGF-II was inversely related in different hepatoma cell lines. PTEN expression induced decreased Sp1 DNA binding by dephosphorylating Sp1 and interfered with transcriptional transactivation of IGF-II by HBx in hepatoma cells. The protein phosphatase activity was involved in PTEN downregulation of IGF-II transcription through downregulation of MAPK, MAPK kinase phosphorylation and PKC translocation. 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