长非编码RNA（LncRNA）参与表观遗传调控等多种生物学过程。其异常在肿瘤发生中扮演重要角色。我们发现并初步鉴定了HANT（HRK-associated noncoding transcripts）这样一组上调Bcl-2家族促凋亡基因HRK的新的lncRNA，在预实验基础上提出如下假说：HANT通过"结合/募集组蛋白修饰酶调节组蛋白修饰"和/或"结合/募集转录因子或辅因子"的机制，或二者的协同作用，促进凋亡调控基因HRK表达。本项目着重探究HANT是否结合并募集组蛋白甲基化酶(如MLL)或乙酰基转移酶（HAT），促进HRK启动子区组蛋白H3K4等的甲基化或组蛋白乙酰化；或结合并募集转录因子（如JUN）；或介导组蛋白修饰与转录因子募集的协同作用，最终激活HRK基因转录。项目亦将分析HANT-HRK调控紊乱与前列腺癌细胞生物学行为及临床病理特点的关系，为其临床应用打基础。

Long non-coding RNAs (lncRNA) participates in many biological processes such as epigenetic regulation, and their abnormalities may play important roles in neoplasia. We identified a novel group of lncRNA desiganted as HANTs (HRK-associated noncoding transcripts ) that upregulates the Bcl-2 family proapoptotic gene HRK. Based on our experimental data, we propose that HANTs upregulate HRK by binding/recruiting histone modifying enzymes and/or transcription factors or co-activators. We will focus on analyzing whether HANTs bind/recruit histone methyltransferases such as MLL and/or histone acetylases, or HRK transcription factors such as JUN, or both, to facilitate HRK gene expression. We will also analyze the relationship between HANT-HRK deregulation with prostate cancer cell biology and patient data to investigate its potential clinical use in the future.