口腔鳞状细胞癌（OSCC）糖酵解异常与OSCC发生发展密切相关，但其具体功能与机制尚不明确。我们前期工作发现：lncRNA-p15135在OSCC癌组织中显著高表达，miR-378a则显著低表达，且两者表达显著相关；沉默lncRNA-p15135或过表达miR-378a可显著抑制OSCC细胞糖酵解及增殖；miR-378a可结合lncRNA-p15135，并对其表达具有明显抑制作用。基于此，我们提出科学假说：lncRNA-p15135通过诱捕miR-378a从而抑制miR-378a对靶mRNA的表达抑制作用，进而共同参与调控OSCC糖酵解，并最终影响OSCC发生发展进程。为验证该假说，本项目将深入阐述lncRNA-p15135-miR-378a信号轴对OSCC糖酵解的具体调控功能、机制及其临床意义。项目将率先揭示lncRNA调控OSCC发生发展新机制，并为OSCC的诊疗提供新思路及理论依据。

Although it has been well known that the deregulation of glycolysis could probably lead to the initiation and development of oral squamous cell carcinoma (OSCC), the exact mechanism remains unclear. Our previous studies had suggested that lncRNA-p15135 was significantly increased in the OSCC tissue samples, and miR-378a was significantly decreased. Moreover, the expression of lncRNA-p15135 was correlated with miR-378a expression level. Functional experiment showed that silencing lncRNA-p15135 in OSCC cells could repress both glycolysis and proliferation. A similar effect was observed by increasing miR-378a expression in OSCC cells. Furthermore, there was a predicted binding site of miR-378a on lncRNA-p15135. LncRNA-p15135 expression was significantly repressed when increasing miR-378a in OSCC cells. These results indicated that lncRNA-p15135 might regulate the expression of targeted mRNA of miR-378a by capturing miR-378a in OSCC cells. This interaction might have downstream effects on glycolysis in OSCC cells, which in turn act as the driver for OSCC initiation and development. In this study, we will explore the functional role and mechanisms of lncRNA-p15135-miR-378a signaling axis on glycolysis of OSCC cells. Meanwhile, we will analyze the clinical relevance of lncRNA-p15135 and miR-378a. In summary, this study would uncover the role of lncRNA-miRNA in OSCC glycolysis, and it will provide a novel strategy of diagnosis and treatment of OSCC.