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10.1158/0008-5472.CAN-14-0225 http://scihub22266oqcxt.onion/10.1158/0008-5472.CAN-14-0225 C4851164!4851164 !25189528     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=25189528 &cmd=llinks): Failed to open stream: HTTP request failed! 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Network modeling of TGF? signaling in hepatocellular carcinoma epithelial-to-mesenchymal transition reveals joint sonic hedgehog and Wnt pathway activation |pdf=|usr=}}{{25189528 }} gab.com Text Network modeling of TGF signaling in hepatocellular carcinoma epithelial-to-mesenchymal transition reveals joint sonic hedgehog and Wnt pathway activation JO: Cancer Res http://www.kidney.de/pget.php?&tw=1&pmid=25189528 #FOAvip Epithelial-to-mesenchymal transition (EMT) is a developmental process hijacked by cancer cells to leave the primary tumor site, invade surrounding tissue, and establish distant metastases. A hallmark of EMT is the loss of E-cadherin expression, and one major signal for the induction of EMT is TGF?, which is dysregulated in up to 40% of hepatocellular carcinoma (HCC). We have constructed an EMT network of 70 nodes and 135 edges by integrating the signaling pathways involved in developmental EMT and known dysregulations in invasive HCC. We then used discrete dynamic modeling to understand the dynamics of the EMT network driven by TGF?. Our network model recapitulates known dysregulations during the induction of EMT and predicts the activation of the Wnt and Sonic hedgehog (SHH) signaling pathways during this process. We show, across multiple murine (P2E and P2M) and human HCC cell lines (Huh7, PLC/PRF/5, HLE, and HLF), that the TGF? signaling axis is a conserved driver of mesenchymal phenotype HCC and confirm that Wnt and SHH signaling are induced in these cell lines. Furthermore, we identify by network analysis eight regulatory feedback motifs that stabilize the EMT process and show that these motifs involve cross-talk among multiple major pathways. Our model will be useful in identifying potential therapeutic targets for the suppression of EMT, invasion, and metastasis in HCC. Twit Text FOAVip Network modeling of TGF signaling in hepatocellular carcinoma epithelial-to-mesenchymal transition reveals joint sonic hedgehog and Wnt pathway activation ????Cancer Res http://www.kidney.de/pget.php?&tw=1&pmid=25189528 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25189528 #FOAvip English Wikipedia <ref>{{Cite pmid|25189528 }}</ref> Network modeling of TGF? signaling in hepatocellular carcinoma epithelial-to-mesenchymal transition reveals joint sonic hedgehog and Wnt pathway activation #MMPMID25189528 Steinway SN ; Zaņudo JG ; Ding W ; Rountree CB ; Feith DJ ; Loughran TP Jr ; Albert R Cancer Res 2014[Nov]; 74 (21 ): 5963-77 PMID25189528 show ga Epithelial-to-mesenchymal transition (EMT) is a developmental process hijacked by cancer cells to leave the primary tumor site, invade surrounding tissue, and establish distant metastases. A hallmark of EMT is the loss of E-cadherin expression, and one major signal for the induction of EMT is TGF?, which is dysregulated in up to 40% of hepatocellular carcinoma (HCC). We have constructed an EMT network of 70 nodes and 135 edges by integrating the signaling pathways involved in developmental EMT and known dysregulations in invasive HCC. We then used discrete dynamic modeling to understand the dynamics of the EMT network driven by TGF?. Our network model recapitulates known dysregulations during the induction of EMT and predicts the activation of the Wnt and Sonic hedgehog (SHH) signaling pathways during this process. We show, across multiple murine (P2E and P2M) and human HCC cell lines (Huh7, PLC/PRF/5, HLE, and HLF), that the TGF? signaling axis is a conserved driver of mesenchymal phenotype HCC and confirm that Wnt and SHH signaling are induced in these cell lines. Furthermore, we identify by network analysis eight regulatory feedback motifs that stabilize the EMT process and show that these motifs involve cross-talk among multiple major pathways. Our model will be useful in identifying potential therapeutic targets for the suppression of EMT, invasion, and metastasis in HCC. |Animals [MESH] |Cadherins/genetics [MESH] |Carcinoma, Hepatocellular/*genetics/pathology [MESH] |Cell Line, Tumor [MESH] |Epithelial-Mesenchymal Transition/genetics [MESH] |Gene Regulatory Networks [MESH] |Hedgehog Proteins/biosynthesis/*genetics [MESH] |Humans [MESH] |Liver Neoplasms/*genetics/pathology [MESH] |Mice [MESH] |Transcriptional Activation/genetics [MESH] |Transforming Growth Factor beta/*genetics [MESH]Network modeling of TGF? signaling in hepatocellular carcinoma epith(epmc).pdf DeepDyve Pubget Overpricing