紫外线B（UVB）是皮肤癌最重要的危险因子，而两极上空臭氧层空洞形成将使地球表面的生物受到紫外辐射日益严重的作用并造成对人类自身及其生存环境的不断危害。本项目拟以现有工作为基础，分别从转录水平、转录后水平以及时空特异性与动态变化调控等层次研究课题组发现的皮肤鳞癌的oncomiR-365在皮肤鳞癌发生发展中的作用及其机制。主要包括：①.使用ChIP-seq和EMSA等技术研究UVB经由转录因子对miR-365的启动子进行调控的机制；②.使用肿瘤细胞生物学方法研究miR-365/NFIB导致HaCaT和A431等细胞生物学行为的变化及其机制，同时研究NFIB的信号转导机制并在临床样本进行验证；③.NFIB负反馈调控miR-365的机制。本项目将为CSCC这一第二高发的皮肤癌症的预防和靶向治疗提供理论基础和实验依据。同时也为方兴未艾的miRNA在肿瘤发生发展中作用机制的研究提供一定的理论基础。

Ultravuilet B (UVB) is the most important skin cancer inducing factor. organisms, include human beings, on the Earth’s surface will be damaged by Increased UV radiation caused by ozone hole over the poles. This project, based on existing work, will study on the mechanism of HaCaT’s transformation to malignant behavior at the transcription, post-transcription and time and space specificity and dynamic change levels. ① the regulation mechanism of UVB on miR-365 promoter by transcription factors by ChIP-seq and EMSA. ② The biologic variation of HaCaT and A431 caused by miR-365 / NFIB and the signal transductional mechanism of NFIB. ③. The mechanism of NFIB negative feedback regulation on miR-365 expression. This project will provide the theoretical basis and experimental evidence for CSCC, the second highest incidence of skin cancer, prevention and treatment and also provide a theoretical basis for the study of the role of miRNA in the development of tumor.