长链非编码RNA-MALAT1在大肠癌转移中起重要作用，但MALAT1表达调控的机制尚不清楚。我们前期研究发现MALAT1激活β-catenin信号通路促进大肠癌转移，MALAT1和β-arrestin表达呈正相关，COX-2/PGE2通过EP2受体上调MALAT1。据此提出“EP2通过介导β-arrestin调节MALAT1激活β-catenin促进大肠癌转移”的科学假说。 .本研究与美国南佛罗里达大学合作，采用CRISPER/cas9基因编辑等技术，研究EP2受体通过β-arrestin介导MALAT1激活β-catenin促进大肠癌转移的机制；构建主动识别EP2受体的新型中药靶向给药系统丹参酮ⅡA纳米粒，探讨丹参酮ⅡA纳米通过靶向EP2抑制β-arrestin/MALAT1/β-catenin通路防治大肠癌转移的机制。这对于揭示大肠癌转移的机制，探索大肠癌的分子靶向治疗具有重要意义。

Long non-coding RNA-MALAT1 plays a key role in the metastasis of human colorectal cancer (CRC), but the underlying regulation mechanism of MALAT1 expression remains elusive. Our preliminary data have shown that MALAT1 activated the β-catenin signaling pathway, resulting in increased CRC metastasis. We also found that MALAT1 expression correlated with that of β-arrestin expression, and COX-2/PGE2 enhanced MALAT1 expression via their binding to EP2 receptor. Hence we here propose the EP2 receptor regulates colorectal cancer metastasis via β-arrestin mediated MALAT1.. In this proposed research project, we will collaborate with University of South Florida in the US, use the CRISPR/cas9 genomic editing technology, to study the mechanism of EP2 receptor regulates colorectal cancer metastasis via β-arrestin mediated MALAT1. Moreover, we will develop a novel traditional Chinese medicine (TCM) drug delivery system of Tanshinone IIA (TSIIA) nanoparticles to target the EP2 receptor actively, and investigate the effect mechanism of TSIIA nanoparticles on the β-arrestin/MALAT1/β-catenin signaling pathway via targeting the EP2 receptror. In summary, our study will help understanding the mechanisms of CRC invasion and metastasis as well as providing new molecular targeting therapy strategy.