IMP3是一类参与RNA转录后调控的RNA结合蛋白，目前在口腔鳞癌中的作用机制尚不清楚。前期通过RIP-seq和生物信息学分析表明转录因子E2F5是IMP3潜在靶点，两者在口腔鳞癌组织中异常高表达并呈正相关；进一步分析发现E2F5mRNA存在多个IMP3特异性结合位点和m6A甲基化修饰位点，且两者有部分重叠；通过干涉IMP3引起E2F5表达下调并抑制口腔鳞癌细胞的增殖。综上提出假说：IMP3通过结合E2F5-m6A靶点调控其表达进而参与口腔鳞癌增殖。本研究拟收集口腔鳞癌组织样本，应用qRT-PCR、免疫组化等方法分析IMP3和E2F5表达的临床意义；MeRIP-PCR、RIP和Pull-down等技术分析IMP3识别和结合E2F5-m6A修饰的分子机制，并通过细胞行为学实验及动物模型揭示其对口腔鳞癌细胞增殖的影响，为阐述IMP3在口腔鳞癌发展中的失调及作用机制与寻求潜在治疗靶点提供新视角。

IMP3 is a class of RNA-binding proteins involved in post-transcriptional regulation of RNA, and its mechanism in oral squamous cell carcinoma is unclear. RIP-seq and bioinformatics analysis showed that the transcription factor E2F5 is a potential target of IMP3, and they are abnormally highly expressed and positively correlated in oral squamous cell carcinoma tissues; Further analysis revealed that there are multiple IMP3 specific binding sites and m6A methylation modification sites in the E2F5 mRNA, and the two partially overlapped; Interfering with IMP3 caused E2F5 expression to be down-regulated and inhibited the proliferation of oral squamous cell carcinoma. In summary, a hypothesis is proposed: IMP3 is involved in the proliferation of oral squamous cell carcinoma through regulating E2F5 expression by binding to the E2F5-m6A target. This study intends to collect oral squamous cell carcinoma tissue samples and analyze the clinical significance of IMP3 and E2F5 expression using qRT-PCR, immunohistochemistry and other methods. Using MeRIP-PCR, RIP, and Pull-down techniques to analyze the molecular mechanism of IMP3 by recognizing and binding E2F5-m6A modification, and reveal its effect on the proliferation of oral squamous cell carcinoma through cell functional experiments and animal models. To provide a new perspective for explaining the dysregulation and mechanism of IMP3 in the development of oral squamous cell carcinoma and seeking potential therapeutic targets.