口腔癌的进程与RNA结合蛋白调控密切相关。课题组前期实验结果显示，RNA结合蛋白IGF2BP2在口腔癌中显著高表达，且与生物钟基因RORA的mRNA结合。目前研究认为IGF2BP2可在转录后水平抑制mRNA的翻译，促进肿瘤发生、发展。因此我们推测：口腔癌中IGF2BP2可能通过沉默RORA的mRNA翻译，阻断了以RORA为核心的抑癌信号。那么导致IGF2BP2在口腔癌中表达上调的可能分子机制是什么呢？综合测序结果、数据库分析和新的研究进展，我们推测IGF2BP2、RORA、let-7家族之间可能存在反馈循环通路。IGF2BP2通过阻断和反馈阻断抑癌信号RORA/let-7，促进肿瘤的增殖、侵袭和转移。本课题通过深入研究IGF2BP2/RORA/let-7/IGF2BP2反馈循环通路及其下游潜在信号网络，初步揭示RNA结合蛋白IGF2BP2在转录后水平调控口腔癌发生、发展的分子机制。

The progression of oral squamous cell carcinoma is closely related to the regulation of RNA-binding proteins. Our preliminary experimental results showed that RNA-binding protein IGF2BP2 was significantly highly expressed in oral squamous cell carcinoma and combined with the clock gene RORA mRNA. Current research suggests that IGF2BP2 can inhibit mRNA translation at the post-transcriptional level and promote the progress of tumors. Therefore, we hypnotize that IGF2BP2 may block the anti-tumor signal network with RORA as the core by silencing RORA mRNA translation in oral squamous cell carcinoma . So what might be the molecular mechanism that leads to the up-regulation of IGF2BP2 in oral squamous cell carcinoma? Combined with sequencing results, database analysis and new research progress, we speculated that there might be a feedback loop between IGF2BP2, RORA and let-7 family members. IGF2BP2 promotes tumor proliferation, invasion, and metastasis by blocking and feedback blocking tumor suppressor signal RORA/ let-7. Through in-depth study of IGF2BP2/RORA/let-7/IGF2BP2 feedback loop pathway and its downstream potential signal network, this study preliminarily revealed the molecular mechanism of RNA-binding protein regulating the progression of oral squamous cell carcinoma at the post-transcription level.