{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,30]],"date-time":"2026-09-30T05:08:05Z","timestamp":1790744885155,"version":"4.1.0"},"reference-count":51,"publisher":"Springer Science and Business Media LLC","issue":"1","license":[{"start":{"date-parts":[[2018,6,11]],"date-time":"2018-06-11T00:00:00Z","timestamp":1528675200000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0"},{"start":{"date-parts":[[2018,6,11]],"date-time":"2018-06-11T00:00:00Z","timestamp":1528675200000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0"}],"funder":[{"DOI":"10.13039\/100000054","name":"U.S. Department of Health & Human Services | NIH | National Cancer Institute","doi-asserted-by":"publisher","award":["R01DK102597"],"award-info":[{"award-number":["R01DK102597"]}],"id":[{"id":"10.13039\/100000054","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000062","name":"U.S. Department of Health & Human Services | NIH | National Institute of Diabetes and Digestive and Kidney Diseases","doi-asserted-by":"publisher","award":["R01CA159942"],"award-info":[{"award-number":["R01CA159942"]}],"id":[{"id":"10.13039\/100000062","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["link.springer.com"],"crossmark-restriction":false},"short-container-title":["Commun Biol"],"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>Hepatoblastoma (HBL) is a pediatric liver cancer that affects children under the age of three. Reduction of tumor suppressor proteins (TSPs) is commonly seen in liver cancer. However, in our studies we find that aggressive, chemo-resistant HBLs exhibit an elevation of TSPs. HBL patients with a classic phenotype have reduced TSP levels, but patients with aggressive HBL express elevated TSPs that undergo posttranslational modifications, eliminating their tumor suppression activities. Here we identify unique aggressive liver cancer domains (ALCDs) that are activated in aggressive HBL by PARP1-mediated chromatin remodeling leading to elevation of modified TSPs and activation of additional cancer pathways: WNT signaling and \u03b2-catenin. Inhibition of PARP1 blocks activation of ALCDs and normalizes expression of corresponding genes, therefore reducing cell proliferation. Our studies reveal PARP1 activation as a mechanism for the development of aggressive HBL, further suggesting FDA-approved PARP1 inhibitors might be used for treatment of patients with aggressive HBL.<\/jats:p>","DOI":"10.1038\/s42003-018-0077-8","type":"journal-article","created":{"date-parts":[[2018,6,5]],"date-time":"2018-06-05T08:01:36Z","timestamp":1528185696000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":39,"title":["PARP1 activation increases expression of modified tumor suppressors and pathways underlying development of aggressive hepatoblastoma"],"prefix":"10.1038","volume":"1","author":[{"given":"Leila","family":"Valanejad","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ashley","family":"Cast","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mary","family":"Wright","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Karl-Dimiter","family":"Bissig","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Rebekah","family":"Karns","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-7977-9122","authenticated-orcid":false,"given":"Matthew T.","family":"Weirauch","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Nikolai","family":"Timchenko","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2018,6,11]]},"reference":[{"key":"77_CR1","doi-asserted-by":"publisher","first-page":"115","DOI":"10.1158\/1078-0432.CCR-17-0710","volume":"23","author":"JM Kalish","year":"2017","unstructured":"Kalish, J. M. et al. Surveillance recommendations for children with overgrowth syndromes and predisposition to wilms tumors and hepatoblastoma. Clin. Cancer Res. 23, 115\u2013122 (2017).","journal-title":"Clin. Cancer Res."},{"key":"77_CR2","first-page":"1","volume":"1","author":"AD Trobaugh-Lotrario","year":"2017","unstructured":"Trobaugh-Lotrario, A. D., Meyers, R. L., O\u2019Neill, A. F. & Feusner, J. H. Unresectable hepatoblastoma: current perspectives. Hepat. Med. 1, 1\u20136 (2017).","journal-title":"Hepat. Med."},{"key":"77_CR3","doi-asserted-by":"publisher","first-page":"19","DOI":"10.1097\/MOP.0000000000000046","volume":"26","author":"P Czauderna","year":"2014","unstructured":"Czauderna, P. et al. Hepatoblastoma state of the art: pathology, genetics, risk stratification, and chemotherapy. Curr. Opin. Pediatr. 26, 19\u201328 (2014).","journal-title":"Curr. Opin. Pediatr."},{"key":"77_CR4","doi-asserted-by":"publisher","first-page":"696","DOI":"10.1016\/j.juro.2014.03.078","volume":"192","author":"A Meyer.","year":"2014","unstructured":"Meyer. A. et al. The natural history of clinically complete responders to neoadjuvant chemotherapy for urothelial carcinoma of the bladder. J. Urol. 192, 696\u2013701 (2014).","journal-title":"J. Urol."},{"key":"77_CR5","doi-asserted-by":"publisher","first-page":"1312","DOI":"10.1016\/j.jhep.2014.08.009","volume":"61","author":"M Eichenm\u00fcller","year":"2014","unstructured":"Eichenm\u00fcller, M. et al. The genomic landscape of hepatoblastoma and their progenies with HCC-like features. J. Hepatol. 61, 1312\u20131320 (2014).","journal-title":"J. Hepatol."},{"key":"77_CR6","doi-asserted-by":"publisher","first-page":"1589","DOI":"10.15252\/emmm.201707814","volume":"11","author":"S Crippa","year":"2017","unstructured":"Crippa, S. et al. Mutant CTNNB1 and histological heterogeneity define metabolic subtypes of hepatoblastoma. EMBO Mol. Med. 11, 1589\u20131604 (2017).","journal-title":"EMBO Mol. Med."},{"key":"77_CR7","doi-asserted-by":"publisher","first-page":"84","DOI":"10.1016\/j.humpath.2017.10.007","volume":"70","author":"H Lee","year":"2017","unstructured":"Lee, H. et al. General paucity of genomic alteration and low tumor mutation burden in refractory and metastatic hepatoblastoma: comprehensive genomic profiling study. Hum. Pathol. 70, 84\u201391 (2017).","journal-title":"Hum. Pathol."},{"key":"77_CR8","doi-asserted-by":"publisher","first-page":"1686","DOI":"10.1002\/hep.27243","volume":"60","author":"D Jia","year":"2014","unstructured":"Jia, D. et al. Exome sequencing of hepatoblastoma reveals novel mutations and cancer genes in the Wnt pathway and ubiquitin ligase complex. Hepatology 60, 1686\u20131696 (2014).","journal-title":"Hepatology"},{"key":"77_CR9","doi-asserted-by":"publisher","first-page":"1720","DOI":"10.3748\/wjg.14.1720","volume":"14","author":"J Martin","year":"2008","unstructured":"Martin, J. & Dufour, J. F. Tumor suppressor and hepatocellular carcinoma. World J. Gastroenterol. 14, 1720\u20131733 (2008).","journal-title":"World J. Gastroenterol."},{"key":"77_CR10","doi-asserted-by":"publisher","first-page":"1","DOI":"10.3389\/fonc.2014.00109","volume":"4","author":"E Aguirre","year":"2014","unstructured":"Aguirre, E., Renner, O., Narlik-Grassow, M. & Blanco-Aparicio, C. Genetic modeling of PIM proteins in cancer: proviral tagging and cooperation with oncogenes, tumor suppressor genes, and carcinogens. Front. Oncol. 4, 1\u201317 (2014).","journal-title":"Front. Oncol."},{"key":"77_CR11","doi-asserted-by":"publisher","first-page":"27","DOI":"10.17140\/CSMMOJ-1-104","volume":"1","author":"NA Timchenko","year":"2015","unstructured":"Timchenko, N. A. & Lewis, K. Elimination of tumor suppressor proteins during liver carcinogenesis. Cancer Stud. Mol. Med. 1, 27\u201338 (2015).","journal-title":"Cancer Stud. Mol. Med."},{"key":"77_CR12","doi-asserted-by":"publisher","first-page":"1098","DOI":"10.1002\/hep.26146","volume":"57","author":"Y Jiang","year":"2013","unstructured":"Jiang, Y. et al. FXR inhibits gankyrin in mouse livers and prevents development of liver cancer. Hepatology 57, 1098\u20131106 (2013).","journal-title":"Hepatology"},{"key":"77_CR13","doi-asserted-by":"publisher","first-page":"e00128","DOI":"10.1128\/MCB.00128-17","volume":"37","author":"K Lewis","year":"2017","unstructured":"Lewis, K. et al. RNA binding protein CUGBP1 inhibits liver cancer in a phosphorylation dependent manner. Mol. Cell. Biol. 37, e00128\u201317 (2017).","journal-title":"Mol. Cell. Biol."},{"key":"77_CR14","doi-asserted-by":"publisher","first-page":"738","DOI":"10.1093\/carcin\/bgx050","volume":"38","author":"L Valanejad","year":"2017","unstructured":"Valanejad, L. et al. FXR-Gankyrin axis is involved in development of pediatric liver cancer. Carcinogenesis 38, 738\u2013747 (2017).","journal-title":"Carcinogenesis"},{"key":"77_CR15","doi-asserted-by":"publisher","DOI":"10.1007\/s10637-017-0474-8","author":"C Wang","year":"2017","unstructured":"Wang, C. & Cheng, L. Gankyrin as a potential therapeutic target for cancer. Invest. New Drugs. https:\/\/doi.org\/10.1007\/s10637-017-0474-8 (2017).","journal-title":"Invest. New Drugs"},{"key":"77_CR16","doi-asserted-by":"publisher","DOI":"10.1038\/cddis.2015.120","volume":"6","author":"X Zhao","year":"2015","unstructured":"Zhao, X. et al. Gankyrin drives malignant transformation of chronic liver damage-mediated fibrosis via the Rac1\/JNK pathway. Cell Death Dis. 6, e1751 (2015).","journal-title":"Cell Death Dis."},{"key":"77_CR17","doi-asserted-by":"publisher","first-page":"1052","DOI":"10.1016\/j.bbrc.2017.06.164","volume":"490","author":"SJ Huang","year":"2017","unstructured":"Huang, S. J. et al. Inducible liver-specific overexpression of gankyrin in zebrafish results in spontaneous intrahepatic cholangiocarcinoma and hepatocellular carcinoma formation. Biochem. Biophys. Res. Commun. 490, 1052\u20131058 (2017).","journal-title":"Biochem. Biophys. Res. Commun."},{"key":"77_CR18","doi-asserted-by":"publisher","first-page":"925","DOI":"10.1016\/j.molcel.2015.04.016","volume":"58","author":"FY Feng","year":"2015","unstructured":"Feng, F. Y., de Bono, J. S., Rubin, M. A. & Knudsen, K. E. Chromatin to clinic: the molecular rationale for PARP1 inhibitor function. Mol. Cell 58, 925\u2013934 (2015).","journal-title":"Mol. Cell"},{"key":"77_CR19","doi-asserted-by":"publisher","first-page":"1134","DOI":"10.1158\/2159-8290.CD-12-0120","volume":"12","author":"MJ Schiewer","year":"2012","unstructured":"Schiewer, M. J. et al. Dual roles of PARP-1 promote cancer growth and progression. Cancer Discov. 12, 1134\u20131149 (2012).","journal-title":"Cancer Discov."},{"key":"77_CR20","doi-asserted-by":"publisher","first-page":"45","DOI":"10.1126\/science.aaf7865","volume":"353","author":"BA Gibson","year":"2016","unstructured":"Gibson, B. A. et al. Chemical genetic discovery of PARP targets reveals a role for PARP-1 in transcription elongation. Science 353, 45\u201350 (2016).","journal-title":"Science"},{"key":"77_CR21","doi-asserted-by":"publisher","first-page":"1126","DOI":"10.1158\/2159-8290.CD-14-0358","volume":"10","author":"JF Goodwin","year":"2014","unstructured":"Goodwin, J. F. & Knudsen, K. E. Beyond DNA repair: DNA-PK function in cancer. Cancer Discov. 10, 1126\u20131139 (2014).","journal-title":"Cancer Discov."},{"key":"77_CR22","doi-asserted-by":"publisher","first-page":"8914","DOI":"10.1093\/nar\/gku591","volume":"42","author":"SJ Roper","year":"2014","unstructured":"Roper, S. J. et al. ADP-ribosyltransferases Parp1 and Parp7 safeguard pluripotency of ES cells. Nucleic Acids Res. 42, 8914\u20138927 (2014).","journal-title":"Nucleic Acids Res."},{"key":"77_CR23","doi-asserted-by":"publisher","first-page":"4492","DOI":"10.1128\/MCB.00160-13","volume":"33","author":"C Wang","year":"2013","unstructured":"Wang, C. et al. Poly(ADP-ribose) polymerase 1 promotes oxidative-stress-induced liver cell death via suppressing farnesoid X receptor \u03b1. Mol. Cell. Biol. 33, 4492\u20134503 (2013).","journal-title":"Mol. Cell. Biol."},{"key":"77_CR24","doi-asserted-by":"publisher","first-page":"8460","DOI":"10.1038\/sj.onc.1206897","volume":"22","author":"C Simbulan-Resenthal","year":"2003","unstructured":"Simbulan-Resenthal, C. et al. PARP1 binds E2F-1 independently on its DNA binding and catalytic domains, and acts as a novel coactivator of E2F1-mediated transcription during re-entry of quiescent cells into S phase. Oncogene 22, 8460\u20138471 (2003).","journal-title":"Oncogene"},{"key":"77_CR25","doi-asserted-by":"publisher","first-page":"102575","DOI":"10.1371\/journal.pone.0102575","volume":"9","author":"C Mostocotto","year":"2014","unstructured":"Mostocotto, C. et al. Poly(ADP-ribosyl)ation is required to modulate chromatin changes at c-MYC promoter during emergence from quiescence. PLoS ONE 9, 102575 (2014).","journal-title":"PLoS ONE"},{"key":"77_CR26","doi-asserted-by":"publisher","first-page":"13770","DOI":"10.1073\/pnas.0906920106","volume":"106","author":"AJ Gottschalk","year":"2009","unstructured":"Gottschalk, A. J. et al. Poly(ADP-ribosyl)ation directs recruitment and activation of an ATP-dependent chromatin remodeler. Proc. Natl Acad. Sci. USA 106, 13770\u201313774 (2009).","journal-title":"Proc. Natl Acad. Sci. USA"},{"key":"77_CR27","doi-asserted-by":"publisher","first-page":"82872","DOI":"10.1371\/journal.pone.0082872","volume":"8","author":"L Yang","year":"2013","unstructured":"Yang, L. et al. Identification of poly(ADP-ribose) polymerase-1 as a cell cycle regulator through modulating Sp1 mediated transcription in human hepatoma cells. PLoS ONE 8, 82872 (2013).","journal-title":"PLoS ONE"},{"key":"77_CR28","volume":"23","author":"D Yao","year":"2013","unstructured":"Yao, D., Pengm, S. & Daim, C. The role of hepatocyte nuclear factor 4alpha in metastatic tumor formation of hepatocellular carcinoma and its close relationship with the mesenchymal-epithelial transition markers. BMC Cancer 23, 413 (2013). 432.","journal-title":"BMC Cancer"},{"key":"77_CR29","doi-asserted-by":"publisher","first-page":"912","DOI":"10.1101\/gad.1183304","volume":"18","author":"GL Wang","year":"2004","unstructured":"Wang, G.-L., Iakova, P., Wilde, M., Awad, S. & Timchenko, N. A. Liver tumors escape negative control of proliferation via PI3K\/Akt-mediated block of C\/EBP\u03b1 growth inhibitory activity. Genes Dev. 18, 912\u2013925 (2004).","journal-title":"Genes Dev."},{"key":"77_CR30","doi-asserted-by":"publisher","first-page":"1325","DOI":"10.1128\/MCB.25.4.1325-1338.2005","volume":"25","author":"GL Wang","year":"2005","unstructured":"Wang, G.-L. & Timchenko, N. A. Dephosphorylated C\/EBP\u03b1 accelerates cell proliferation through sequestering retinoblastoma protein. Mol. Cell. Biol. 25, 1325\u20131338 (2005).","journal-title":"Mol. Cell. Biol."},{"key":"77_CR31","doi-asserted-by":"publisher","first-page":"2549","DOI":"10.1172\/JCI41933","volume":"120","author":"GL Wang","year":"2010","unstructured":"Wang, G.-L. et al. Elimination of C\/EBP\u03b1 through the ubiquitin-proteasome system promotes the development of liver cancer in mice. J. Clin. Invest. 120, 2549\u20132562 (2010).","journal-title":"J. Clin. Invest."},{"key":"77_CR32","doi-asserted-by":"publisher","first-page":"65","DOI":"10.1016\/j.jhep.2012.08.023","volume":"58","author":"AM Cozzolino","year":"2013","unstructured":"Cozzolino, A. M. et al. TGF\u03b2 overrides HNF4\u03b1 tumor suppressing activity through GSK3\u03b2 inactivation: implication for hepatocellular carcinoma gene therapy. J. Hepatol. 58, 65\u201372 (2013).","journal-title":"J. Hepatol."},{"key":"77_CR33","doi-asserted-by":"publisher","first-page":"239","DOI":"10.1016\/j.cmet.2005.09.003","volume":"2","author":"A Abella","year":"2015","unstructured":"Abella, A. et al. Cdk4 promotes adipogenesis through PPARgamma activation. Cell Metab. 2, 239\u2013249 (2015).","journal-title":"Cell Metab."},{"key":"77_CR34","doi-asserted-by":"publisher","first-page":"71","DOI":"10.1007\/978-94-017-9211-0_4","volume":"85","author":"C Vaughan","year":"2014","unstructured":"Vaughan, C., Pearsall, I., Yeudall, A., Deb, S. P. & Deb, S. p53: its mutations and their impact on transcription. Subcell. Biochem. 85, 71\u201390 (2014).","journal-title":"Subcell. Biochem."},{"key":"77_CR35","doi-asserted-by":"publisher","first-page":"15532","DOI":"10.1073\/pnas.1411746111","volume":"111","author":"MG Lee","year":"2014","unstructured":"Lee, M. G. et al. XAF1 directs apoptotic switch of p53 signaling through activation of HIPK2 and ZNF313. Proc. Natl Acad. Sci. USA 111, 15532\u201315537 (2014).","journal-title":"Proc. Natl Acad. Sci. USA"},{"key":"77_CR36","doi-asserted-by":"publisher","first-page":"1481","DOI":"10.1016\/j.celrep.2016.04.032","volume":"15","author":"L Tortola","year":"2016","unstructured":"Tortola, L. et al. The tumor suppressor Hace1 is a critical regulator of TNFR1-mediated cell fate. Cell Rep. 15, 1481\u20131492 (2016).","journal-title":"Cell Rep."},{"key":"77_CR37","doi-asserted-by":"publisher","first-page":"1430","DOI":"10.1111\/liv.12586","volume":"35","author":"JA Mu\u00f1oz-G\u00e1mez","year":"2015","unstructured":"Mu\u00f1oz-G\u00e1mez, J. A. et al. Synergistic cytotoxicity of the poly (ADP-ribose) polymerase inhibitor ABT-888 and temozolomide in dual-drug targeted magnetic nanoparticles. Liver Int. 35, 1430\u20131441 (2015).","journal-title":"Liver Int."},{"key":"77_CR38","doi-asserted-by":"publisher","first-page":"255","DOI":"10.1002\/hep.23249","volume":"51","author":"R Quiles-Perez","year":"2010","unstructured":"Quiles-Perez, R. et al. Inhibition of poly adenosine diphosphate-ribose polymerase decreases hepatocellular carcinoma growth by modulation of tumor-related gene expression. Hepatology 51, 255\u2013266 (2010).","journal-title":"Hepatology"},{"key":"77_CR39","doi-asserted-by":"publisher","DOI":"10.1002\/hep.29677","author":"A Cast","year":"2017","unstructured":"Cast, A. et al. C\/EBP\u03b1-dependent pre-neoplastic tumor foci are the origin of hepatocellular carcinoma and aggressive pediatric liver cancer. Hepatology. https:\/\/doi.org\/10.1002\/hep.29677 (2017).","journal-title":"Hepatology"},{"key":"77_CR40","doi-asserted-by":"publisher","first-page":"860","DOI":"10.1038\/35057062","volume":"15","author":"ES Landers","year":"2001","unstructured":"Landers, E. S. et al. Initial sequencing and analysis of the human genome. Nature 15, 860\u2013921 (2001).","journal-title":"Nature"},{"key":"77_CR41","doi-asserted-by":"publisher","first-page":"68","DOI":"10.1016\/S0168-9525(02)00006-9","volume":"19","author":"IK Jordan","year":"2003","unstructured":"Jordan, I. K., Rogozin, I. B., Glazko, G. V. & Koonin, E. V. Origin of a substantial fraction of human regulatory sequences from transposable elements. Trends Genet. 19, 68\u201372 (2003).","journal-title":"Trends Genet."},{"key":"77_CR42","doi-asserted-by":"publisher","first-page":"7056","DOI":"10.1128\/MCB.13.11.7056","volume":"13","author":"JE Hambor","year":"1993","unstructured":"Hambor, J. E., Mennone, J., Coon, M. E., Hanke, J. H. & Kavathas, P. Identification and characterization of an Alu-containing, T-cell-specific enhancer located in the last intron of the human CD8 alpha gene. Mol. Cell. Biol. 13, 7056\u20137070 (1993).","journal-title":"Mol. Cell. Biol."},{"key":"77_CR43","doi-asserted-by":"publisher","first-page":"836","DOI":"10.1038\/ng.2649","volume":"45","author":"M Xie","year":"2013","unstructured":"Xie, M. et al. DNA hypomethylation within specific transposable element families associates with tissue-specific enhancer landscape. Nat. Genet. 45, 836\u2013841 (2013).","journal-title":"Nat. Genet."},{"key":"77_CR44","doi-asserted-by":"publisher","first-page":"891","DOI":"10.1074\/jbc.273.2.891","volume":"9","author":"Z Yang","year":"1998","unstructured":"Yang, Z., Boffelli, D., Boonmark, N., Schwartz, K. & Lawn, R. Apolipoprotein(a) gene enhancer resides within a LINE element. J. Biol. Chem. 9, 891\u2013897 (1998).","journal-title":"J. Biol. Chem."},{"key":"77_CR45","doi-asserted-by":"publisher","first-page":"87","DOI":"10.1038\/nature04696","volume":"4","author":"G Bejerano","year":"2006","unstructured":"Bejerano, G. et al. A distal enhancer and an ultraconserved exon are derived from a novel retroposon. Nature 4, 87\u201390 (2006).","journal-title":"Nature"},{"key":"77_CR46","doi-asserted-by":"publisher","first-page":"397","DOI":"10.1038\/nrg2337","volume":"9","author":"C Feschotte","year":"2008","unstructured":"Feschotte, C. Transposable elements and the evolution of regulatory networks. Nat. Rev. Genet. 9, 397\u2013405 (2008).","journal-title":"Nat. Rev. Genet."},{"key":"77_CR47","doi-asserted-by":"publisher","first-page":"1998","DOI":"10.1002\/hep.26763","volume":"59","author":"P Mukhopadhyay","year":"2014","unstructured":"Mukhopadhyay, P. et al. Poly (ADP-ribose) polymerase-1 is a key mediator of liver inflammation and fibrosis. Hepatology 59, 1998\u20132009 (2014).","journal-title":"Hepatology"},{"key":"77_CR48","doi-asserted-by":"publisher","first-page":"589","DOI":"10.1016\/j.jhep.2016.10.023","volume":"66","author":"P Mukhapadhyay","year":"2017","unstructured":"Mukhapadhyay, P. et al. PARP inhibition protects against alcoholic and non-alcoholic steatohepatitis. J. Hepatol. 66, 589\u2013600 (2017).","journal-title":"J. Hepatol."},{"key":"77_CR49","doi-asserted-by":"publisher","first-page":"325","DOI":"10.1016\/j.jhep.2016.04.009","volume":"65","author":"B Bissig-Choisat","year":"2016","unstructured":"Bissig-Choisat, B. et al. Novel patient-derived xenograft and cell line models for therapeutic testing of pediatric liver cancer. J. Hepatol. 65, 325\u2013333 (2016).","journal-title":"J. Hepatol."},{"key":"77_CR50","doi-asserted-by":"publisher","first-page":"329","DOI":"10.1038\/nprot.2007.30","volume":"2","author":"C Liang","year":"2007","unstructured":"Liang, C., Park, A. & Guan, J. In Vitro scratch assay: a convenient and inexpensive method for analysis of cell migration in vitro. Nat. Protoc. 2, 329\u2013333 (2007).","journal-title":"Nat. Protoc."},{"key":"77_CR51","doi-asserted-by":"publisher","first-page":"28","DOI":"10.1016\/j.semcancer.2010.09.001","volume":"21","author":"P Iakova","year":"2011","unstructured":"Iakova, P., Timchenko, L. T. & Timchenko, N. A. Intracellular signaling and hepatocellular carcinoma. Semin. Cancer Biol. 21, 28\u201334 (2011).","journal-title":"Semin. Cancer Biol."}],"container-title":["Communications Biology"],"original-title":[],"language":"en","link":[{"URL":"https:\/\/www.nature.com\/articles\/s42003-018-0077-8.pdf","content-type":"application\/pdf","content-version":"vor","intended-application":"text-mining"},{"URL":"https:\/\/www.nature.com\/articles\/s42003-018-0077-8","content-type":"text\/html","content-version":"vor","intended-application":"text-mining"},{"URL":"https:\/\/www.nature.com\/articles\/s42003-018-0077-8.pdf","content-type":"application\/pdf","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2022,12,21]],"date-time":"2022-12-21T07:45:17Z","timestamp":1671608717000},"score":1,"resource":{"primary":{"URL":"https:\/\/www.nature.com\/articles\/s42003-018-0077-8"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[2018,6,11]]},"references-count":51,"journal-issue":{"issue":"1","published-online":{"date-parts":[[2018,12]]}},"alternative-id":["77"],"URL":"https:\/\/doi.org\/10.1038\/s42003-018-0077-8","relation":{},"ISSN":["2399-3642"],"issn-type":[{"value":"2399-3642","type":"electronic"}],"subject":[],"published":{"date-parts":[[2018,6,11]]},"assertion":[{"value":"8 November 2017","order":1,"name":"received","label":"Received","group":{"name":"ArticleHistory","label":"Article History"}},{"value":"21 May 2018","order":2,"name":"accepted","label":"Accepted","group":{"name":"ArticleHistory","label":"Article History"}},{"value":"11 June 2018","order":3,"name":"first_online","label":"First Online","group":{"name":"ArticleHistory","label":"Article History"}},{"value":"The authors declare no competing interests.","order":1,"name":"Ethics","group":{"name":"EthicsHeading","label":"Competing interests"}}],"article-number":"67"}}