Nsidered statistically substantial. Each of the statistical tests were performed working with SPSS 20.0 statistical computer software (SPSS Company, Chicago, IL, USA).Acknowledgements This study was supported in element by grants from the National Natural Science Foundation of China (81371866), International Cooperation Project of Guangzhou Science and Technologies Program (2016201604030021), the National Grant System on Essential Infectious Disease (2014ZX10002002-002), Big Project of collaborative Pla2 Inhibitors MedChemExpress innovation of the Guangzhou Science and Technologies Program (201704020175). Author particulars 1 Division of Infectious Diseases, The Third Affiliated Hospital of Sun Yat-sen University, Guangzhou, China. 2Guangdong Province Crucial Laboratory of Liver Disease Study, The Third Affiliated Hospital of Sun Yat-sen University, Guangzhou, China. 3Department of Hepatobiliary Surgery, The Third Affiliated Hospital of Sun Yat-sen University, Guangzhou, ChinaReferences 1. Ferlay, J. et al. Mequinol Technical Information cancer incidence and mortality worldwide: sources, approaches and important patterns in GLOBOCAN 2012. Int. J. Cancer 136, E359 386 (2015). 2. Forner, A., Gilabert, M., Bruix, J. Raoul, J. L. Therapy of intermediate-stage hepatocellular carcinoma. Nat. Rev. Clin. Oncol. 11, 525?35 (2014). 3. Llovet, J. M. et al. Hepatocellular carcinoma. Nat. Rev. Dis. Primers two, 16018 (2016). four. Dawson, M. A. Kouzarides, T. Cancer epigenetics: from mechanism to therapy. Cell 150, 12?7 (2012). five. Huang, Y., Tai, A. W., Tong, S. Lok, A. S. HBV core promoter mutations promote cellular proliferation via E2F1-mediated upregulation of Sphase kinase-associated protein 2 transcription. J. Hepatol. 58, 1068?073 (2013). 6. Huang, Y., Tong, S., Tai, A. W., Hussain, M. Lok, A. S. Hepatitis B virus core promoter mutations contribute to hepatocarcinogenesis by deregulating SKP2 and its target, p21. Gastroenterology 141, 1412?421 (2011). 7. Kops, G. J., Weaver, B. A. Cleveland, D. W. Around the road to cancer: aneuploidy along with the mitotic checkpoint. Nat. Rev. Cancer. five, 773?85 (2005). 8. Liu, X., Gong, H. Huang, K. Oncogenic role of kinesin proteins and targeting kinesin therapy. Cancer Sci. 104, 651?56 (2013). 9. Lawrence, C. J. et al. A standardized kinesin nomenclature. J. Cell. Biol. 167, 19?2 (2004). 10. Miki, H., Setou, M., Kaneshiro, K. Hirokawa, N. All kinesin superfamily protein, KIF, genes in mouse and human. Proc. Natl Acad. Sci.USA 98, 7004?011 (2001). 11. Wu, G. Chen, P. L. Structural specifications of chromokinesin Kif4A for its right function in mitosis. Biochem. Biophys. Res. Commun. 372, 454?58 (2008). 12. Taniwaki, M. et al. Activation of KIF4A as a prognostic biomarker and therapeutic target for lung cancer. Clin. Cancer Res.13, 6624?631 (2007). 13. Minakawa, Y. et al. Kinesin household member 4A: a potential predictor for progression of human oral cancer. PLoS A single eight, e85951 (2013). 14. Narayan, G. et al. Gene dosage alterations revealed by cDNA microarray evaluation in cervical cancer: identification of candidate amplified and overexpressed genes. Genes Chromosomes Cancer 46, 373?84 (2007). 15. Colak, D. et al. Age-specific gene expression signatures for breast tumors and cross-species conserved potential cancer progression markers in young ladies. PLoS 1 8, e63204 (2013). 16. Zou, J. X. et al. Kinesin loved ones deregulation coordinated by bromodomain protein ANCCA and histone methyltransferase MLL for breast cancer cell development, survival, and tamoxifen resistance. Mol. Cancer Res. 12, 539?49 (2014).Official journ.