在肿瘤的发生发展中非编码RNA的表达异常是常见的分子事件，但其表达异常机制并未完全阐明。RNA结合蛋白是在转录或转录后水平上调控RNA生成的最重要因素之一，课题组前期通过RNA-seq发现RBM24是鼻咽癌中最显著下调的RNA结合蛋白，高表达RBM24抑制鼻咽癌细胞增殖和克隆形成能力，并上调miR-25-3p及下调促癌lncRNA-肺腺癌转移相关转录子1(MALAT1)的表达。进而提出在鼻咽癌中RBM24可能通过调控miR-25-3p的生成来抑制MALAT1分子从而抑制肿瘤进展的假说。为此，我们拟证实RBM24蛋白通过与pre-miR-25结合调控miR-25的生成；确定MALAT1是miR-25-3p的关键靶基因；阐明RBM24、miR-25-3p和MALAT1在蛋白、miRNA及lncRNA不同类型分子信息传递的复杂网络中各调控关系，以及它们在鼻咽癌中的生物学功能与临床病理学意义。

Deregulation of non-coding RNA was demonstrated to be a common molecular even in various human cancers, but the underlying mechanism has not been well documented. RNA binding protein is one of the key regulators in mediating RNA transcription and post-transcription processing. To demonstrate the role of RNA binding protein in nasopharyngeal carcinoma, we did RNA-seq and identified RBM24 was the most down-regulated RNA-binding protein. Overexpression of RBM24 could inhibit proliferation and colony formation ability of nasopharyngeal carcinoma cells, and enhance the expression of miR-25-3p and inhibit the pro-oncogenic lncRNA- MALAT1 (metastasis associated lung adenocarcinoma transcript 1).Thus, we hypothesize that RBM24 acts as a tumor suppressor in nasopharyngeal carcinoma by directly interacting with pre-miR-25 and enhancing its processing, which result in the inhibition of MALAT1 by miR-25-3p.To confirm this hypothesis, we will study the interaction of RBM24 and pre-miR-25 and their interaction domain; illustrate whether MALAT1 is a key target of miR-25-3p and the regulations of RBM24, miR-25-3p and MALAT1 among the protein, miRNA and lncRNA network. Finally, we hope to demonstrate the functional and clinical significance of RBM24, miR-25-3p and MALAT1 in nasopharyngeal carcinomas.