RNA甲基化（m6A）是生命活动中极为重要的表观遗传调控方式，但其在胰腺癌中的作用和机制至今未见报道。我们发现：胰腺癌中m6A水平和m6A甲基化酶METTL3显著高于正常组织，METTL3在胰腺癌成瘤和侵袭转移中发挥重要作用；表达谱芯片提示：METTL3干预后可能调控Rap1B基因，导致下游ERK等信号通路分子激活影响胰腺癌恶性生物学行为。但在胰腺癌中m6A现象及其详细分子机制仍未彻底的阐明，因此，本项目拟：运用MeRIP-Seq技术检测胰腺癌中m6A谱，探明m6A关键酶的表达和功能；阐明METTL3调控Rap1B的详细分子机制；明确METTL3调控Rap1B后对下游信号通路的影响。本项目首次阐明胰腺癌m6A现象及其分子调控机制，有望从m6A的角度揭示胰腺癌生物学行为的分子机制，为胰腺癌治疗打下基础。

N6-methyladenosine is one of the most prevalent and important epigenetic regulation in the life. However, the affection and mechanism of m6A in pancreatic cancer have not been reported till now. Our preliminary data found that the leval of m6A and the expression of the methyltransferase METTL3 were higher in pancreatic cancer than in normal pancrease. The detection by gene microarray showed that METTL3 may regulate the Rap1B gene, which may activate the downstream cell signaling pathways, such as ERK pathway. But till now, the expression and mechanism of m6A in pancreatic cancer are still unclear and need further researches. Here, we will detect the m6A gene profiles of pancreatic cancer. Then, we will explore the expression and affection of m6A methyltransferase and demethylases in pancreatic cancer. Furthermore, we will demonstrate the dysregulated mechanism of Rap1B by METTL3. Last, we will detect the downstream signaling pathways after METTL3-Rap1B regulated. It is the first time to demonstrate the expression, affection and mechanism of m6A in pancreatic cancer. This research may further reveal the molecular mechanism of the pancreatic cancer through m6A, which would provide new therapy strategy.