RNA m6A甲基化是重要的转录后修饰方式，与多种肿瘤发展密切相关，但其调控机制有待深入探索。甲基化转移酶样蛋白（METTL）是最近发现的甲基化修饰基因家族，调控多种细胞功能。我们前期研究发现该家族成员METTL7B在非小细胞肺癌（NSCLC）中表达显著升高且与预后负相关；过表达METTL7B加速肺癌细胞生长并上调其整体RNA m6A水平；转录组测序筛选并经细胞实验证实METTL7B可显著上调重要促癌基因-长链非编码RNA NEAT1。我们推测：METTL7B可能通过m6A甲基化修饰上调NEAT1从而促进肺癌细胞生长。我们拟通过体内外实验验证METTL7B-NEAT1调控轴对NSCLC生长的影响，利用Me-RIP、CLIP、基因编辑等技术剖析METTL7B调控NEAT1 m6A甲基化的详细分子机制和过程，为揭示其介导的非编码RNA表观遗传调控机制在NSCLC发生发展中的作用提供理论基础。

RNA m6A methylation is an important post-transcriptional modification, which is closely related to the development of various tumors,however, the underlying regulatory mechanism remains to be further explored. Recently, Methyltransferase-like proteins (METTL) are found to be a family of proteins that regulate a variety of cellular functions. Our previous study found that the expression of METTL7B in non-small cell lung cancer (NSCLC) was significantly increased and negatively correlated with prognosis. Overexpression of METTL7B accelerated the growth of lung cancer cells along with up-regulated the overall RNA m6A level. Transcriptome sequencing screening and cell experiments confirmed that METTL7B significantly up-regulated the important oncogene - long non-coding RNA NEAT1.We speculate that METTL7B may promote the growth of lung cancer cells by increasing NEAT1 by m6A methylation regulation.This project intends to further verify the effect of METTL7B-NEAT1 regulatory axis on the proliferation phenotype of NSCLC in vivo and in vitro.The detailed molecular mechanism of METTL7B in regulating the methylation of NEAT1 m6A was also explored by using Me-RIP, CLIP and gene editing technologies .This project will provide theoretical basis for elucidating the role of non-coding RNA epigenetic regulatory mechanism mediated by METTL7B in the development of NSCLC.