Nsidered statistically significant. All the statistical tests were performed employing SPSS 20.0 statistical application (SPSS Corporation, Chicago, IL, USA).Acknowledgements This study was supported in component by grants from the National Natural Science Foundation of China (81371866), International Cooperation Project of Guangzhou Science and Technology Program (2016201604030021), the National Grant Program on Important Infectious Disease (2014ZX10002002-002), Important Project of collaborative innovation from the Guangzhou Science and Technologies System (201704020175). Author particulars 1 Department of Infectious Illnesses, The Third Affiliated Hospital of Sun Yat-sen University, Guangzhou, China. 2Guangdong Province Key Laboratory of Liver Illness Research, 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 important patterns in GLOBOCAN 2012. Int. J. Cancer 136, E359 386 (2015). 2. Forner, A., Gilabert, M., Bruix, J. Raoul, J. L. Remedy of intermediate-stage hepatocellular Lesogaberan MedChemExpress carcinoma. Nat. Rev. Clin. Oncol. 11, 525?35 (2014). 3. 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 market cellular proliferation through 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 along with the mitotic checkpoint. Nat. Rev. Cancer. 5, 773?85 (2005). 8. 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?2 (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 requirements of chromokinesin Kif4A for its proper 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 loved ones member 4A: a possible predictor for progression of human oral cancer. PLoS 1 8, 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 prospective cancer progression markers in young females. PLoS 1 8, Chlorpyrifos MedChemExpress 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.