Nsidered statistically important. All of the statistical tests have been performed working with SPSS 20.0 statistical computer software (SPSS Enterprise, Chicago, IL, USA).Acknowledgements This study was supported in component by grants from the National Organic Science Foundation of China (81371866), International Cooperation Project of Guangzhou Science and Technologies System (2016201604030021), the National Grant Plan on Key Infectious Illness (2014ZX10002002-002), Important Project of collaborative innovation on the Guangzhou Science and Technologies Program (201704020175). Author details 1 Division of Infectious Illnesses, The Third Affiliated Hospital of Sun Quinine (hemisulfate hydrate) Epigenetic Reader Domain Yat-sen University, Guangzhou, China. 2Guangdong Province Important 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. Cancer incidence and mortality worldwide: sources, approaches and significant patterns in GLOBOCAN 2012. Int. J. Cancer 136, E359 386 (2015). 2. Forner, A., Gilabert, M., Bruix, J. Raoul, J. L. Treatment of intermediate-stage hepatocellular carcinoma. Nat. Rev. Clin. Oncol. 11, 525?35 (2014). three. Llovet, J. M. et al. Hepatocellular carcinoma. Nat. Rev. Dis. Primers 2, 16018 (2016). 4. Dawson, M. A. Kouzarides, T. Cancer epigenetics: from mechanism to therapy. Cell 150, 12?7 (2012). 5. Huang, Y., Tai, A. W., Tong, S. Lok, A. S. HBV core promoter mutations promote cellular proliferation by means of E2F1-mediated upregulation of Sphase kinase-associated protein 2 transcription. J. Hepatol. 58, 1068?073 (2013). six. 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. On the road to cancer: aneuploidy plus the mitotic checkpoint. Nat. Rev. Cancer. five, 773?85 (2005). eight. Liu, X., Gong, H. Huang, K. Oncogenic function 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?two (2004). ten. 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 suitable 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 possible predictor for progression of human oral cancer. PLoS A single 8, e85951 (2013). 14. Narayan, G. et al. Gene dosage alterations revealed by cDNA microarray analysis 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 possible cancer progression markers in young girls. PLoS One eight, e63204 (2013). 16. Zou, J. X. et al. Kinesin family deregulation coordinated by bromodomain protein ANCCA and histone methyltransferase MLL for breast cancer cell growth, survival, and tamoxifen resistance. Mol. Cancer Res. 12, 539?49 (2014).Official journ.
