最新研究表明长链非编码RNA(LncRNA)对肿瘤的发生发展及预后起到非常重要的作用。我们前期实验运用LncRNA芯片技术发现LINC00237高表达与肠癌转移密切相关，过表达LINC00237能够促进肠癌细胞的侵袭转移和血管生成能力；荧光素酶实验证实miR-532为LINC00237的靶序列, 而回复miR-532表达能够明显减弱LINC00237诱导的促侵袭转移及血管生成能力。由此我们提出LINC00237促进肠癌转移的新机制：LINC00237作为ceRNA,通过“吸附”互补的miR-532，导致miR-532对下游靶基因的转录后抑制作用减弱，引起下游相关信号通路被激活，促进结直肠癌细胞血管生成和侵袭转移的分子机制。本研究拟通过体内外实验证实LINC00237功能，获得LINC00237抑制miR-532表达，从而激活下游相关信号通路的可靠依据，为肠癌临床分子靶向治疗提供理论参考。

Recent studies revealed that deregulation of long non-coding RNA(LncRNA) played an important role in cancinogenesis, acting as oncogenes or tumor suppressor genes. Our previous LncRNA microarray analysis showed that LINC00237 was overexpressed in colorectal cancer(CRC) tissue and assciated with CRC metastasis. Functional study demonstrated overexpression of LINC00237 in CRC cells decelerated biological activity of motility, invasiveness and angiogenesis. Further luciferase results showed that LINC00237 repressed miR-532 expression directly, while resotration of miR-532 on LINC00237-overexpressing cells counteracts the effect of LINC00237 on tumour metastasis and angiogenesis. Therefore,we propose the new mechanism that LINC00237 modulates miR-532 expression through binding miR-532 directly, thus decreases the inhibitory effect of miR-532 on target genes and downstream signaling pathways, and thus promotes CRC metastasis and angiogenesis. This study is aimed at exploring function and mechanism of LINC00237 in vitro and in vivo, providing theoretical evidence for CRC targeting therapy.