RBM24 suppresses cancer progression by upregulating miR-25 to target MALAT1 in nasopharyngeal carcinoma.
RBM24 suppresses cancer progression by upregulating miR-25 to target MALAT1 in nasopharyngeal carcinoma.
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RBM24 通过上调 miR-25 靶向鼻咽癌中的 MALAT1 来抑制癌症进展
DOI：
10.1038/cddis.2016.252
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发表时间：
2016-09-01
影响因子：
9
通讯作者：
Zeng MS
中科院分区：
文献类型：
--
作者：
Hua WF;Zhong Q;Xia TL;Chen Q;Zhang MY;Zhou AJ;Tu ZW;Qu C;Li MZ;Xia YF;Wang HY;Xie D;Claret FX;Song EW;Zeng MS
非编码RNA之间的异常相互作用已被证明是多种人类癌症中常见的分子事件，但其意义和潜在机制尚未被很好地记录下来。RNA结合蛋白(RBPs)是RNA转录和转录后加工的关键调控因子。在本研究中，我们发现RNA结合蛋白24(RBM24)在鼻咽癌中经常下调。在小鼠模型中，RBM24表达的恢复抑制了鼻咽癌细胞的增殖、迁移和侵袭，并阻止了转移定植。基因芯片分析表明，RBM24表达上调了鼻咽癌细胞miR-25的表达。同样，异位miR-25通过靶向致癌基因LncRNA MALAT1抑制鼻咽癌细胞的生长和运动，而MALAT1表达的下调在鼻咽癌细胞中表现出类似于RBM24恢复的作用。总体而言，这些发现表明了RBM24作为肿瘤抑制因子的新作用。从机制上讲，RBM24至少部分地通过上调miR-25的表达来发挥作用，miR-25反过来又针对MALAT1进行降解。
Abnormal interaction between non-coding RNAs has been demonstrated to be a common molecular event in various human cancers, but its significance and underlying mechanisms have not been well documented. RNA-binding proteins (RBPs) are key regulators of RNA transcription and post-transcriptional processing. In this study, we found that RNA-binding protein 24 (RBM24) was frequently downregulated in nasopharyngeal carcinoma (NPC). The restoration of RBM24 expression suppressed NPC cellular proliferation, migration and invasion and impeded metastatic colonization in mouse models. Microarray analyses revealed that miR-25 expression was upregulated by RBM24 expression in NPC cells. Similarly, ectopic miR-25 expression suppressed NPC cellular growth and motility by targeting the pro-oncogenic lncRNA MALAT1, and the knockdown of MALAT1 expression exhibited similar effects as RBM24 restoration in NPC cells. Overall, these findings suggest a novel role of RBM24 as a tumor suppressor. Mechanistically, RBM24 acts at least in part through upregulating the expression of miR-25, which in turn targets MALAT1 for degradation.
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