长期从事肿瘤转录组学、肿瘤标志物鉴定及作用机制研究工作,在前列腺癌信号传导通路,miRNA对前列腺癌发生发展的作用以及其它非编码RNA的调控机制等方面做出成绩。建立了雄激素受体数据库(Mol Endocrinol, 2009),构建了miRNA介导的AR调控网络(PLoS One. 2013),并对其中其重要作用的miRNA(miR-421、miR-133b、miR-135a等)进行了深入的功能和机制研究(Int J Biochem Cell Biol. 2016, Clinic Cancer Research,2014,Oncotarget,已接收),鉴定并初步验证了一批雄激素反应lncRNA(Oncotarget,修回)。还探讨了AR的转录调控机制,发现KDM1A的去甲基化作用和DNA氧化损伤触发了雄激素诱导的靶基因的表达(Prostate. 2015)。主持863专项,国家科技重大专项,国家自然科学基金等多个重要课题。
Meng D, Yang S, Wan X, Zhang Y, Huang W, Zhao P, Li T, Wang L, Huang Y, Li T, Li Y. A transcriptional target of androgen receptor, miR-421 regulates proliferation and metabolism of prostate cancer cells. Int J Biochem Cell Biol. 2016 Jan 28;73:30-40.
Wan X, Yang S, Huang W, Wu D, Chen H, Wu M, Li J, Li T, Li Y. UHRF1 overexpression is involved in cell proliferation and biochemical recurrence in prostate cancer after radical prostatectomy. J Exp Clin Cancer Res. 2016 Feb 17;35(1):34.
Yang S, Zhang J, Zhang Y, Wan X, Zhang C, Huang X, Huang W, Pu H, Pei C, Wu H, Huang Y, Huang S, Li Y. KDM1A triggers androgen-induced miRNA transcription via H3K4me2 demethylation and DNA oxidation. Prostate. 2015 Jun;75(9):936-46.
Li X, Wan XC, Chen HB, Yang S, Liu YY, Mo WJ, Meng DL, Du WT, Huang Y, Wu H, Wang JQ, Li T, Li Y. Identification of miR-133b and RB1CC1 as independent predictors for biochemical recurrence and potential therapeutic targets for prostate cancer. Clin Cancer Res, 2014 20(9); 2312-2325
Mo W, Zhang J, Li X, Meng D, Gao Y, Yang S, Wan X, Zhou C, Guo F, Huang Y, Amente S, Avvedimento EV, Xie Y, Li Y.Identification of novel AR-targeted microRNAs mediating androgen signalling through critical pathways to regulate cell viability in prostate cancer. PLoS One. 2013;8(2):e56592.
Jiang M, Ma Y, Chen C, Fu X, Yang S, Li X, Yu G, Mao Y, Xie Y, Li Y..Androgen-Responsive Gene Database: Integrated Knowledge on Androgen-Responsive Genes. Mol Endocrinol, 2009, 23(11):1927–1933
Xuechao Wan, Honglei Pu, Wenhua Huang, Shu Yang, Yalong Zhang, Zhe Kong, Zhuoran Yang, Peiqing Zhao, Ao Li , Tao Li, Yao Li. Androgen-induced miR-135a acts as a tumor suppressor through downregulating RBAK and MMP11, and mediates resistance to androgen deprivation therapy. Oncotarget. 已接收