紫外线B（UVB）是上皮细胞鳞癌（CSCC）最重要的致病因子，非编码RNA参与调控CSCC发生的机制是近些年此领域的研究热点之一。本项目基于现有工作基础提出科学假设：MALAT1以ceRNA和直接募集c-MYC从而影响KTN1的表达两种方式、分别从转录后水平和翻译水平上共同调控EGFR来参与UVB诱发CSCC的进程。为此，拟从下述四个方面展开工作：①验证MALAT1以ceRNA功能的形式对EGFR进行转录后调控；②探讨KTN1在CSCC中的抑癌基因功能和对EGFR蛋白表达水平的调控，同时探讨其分子机制；③采用定量蛋白质组学技术分析KTN1的变化对CSCC全组蛋白质表达谱的影响；④构建裸鼠移植瘤模型和转基因小鼠模型用以在整体水平上验证上述体外实验结果。本项目不但能为CSCC的防治提供潜在的分子靶点和理论依据，同时也为非编码RNA在上皮肿瘤发生发展中的调控机制研究提供新的研究思路和理论依据。

Ultraviolet B (UVB) is the most crucial physical carcinogen in cutaneous squamous cell carcinoma(CSCC). The mechanism of non-coding RNA involved in the regulation of CSCC is one of the research hotspots in this field in recent years. This project, based on the existing work, puts forward the scientific hypothesis that MALAT1 participates in UVB-induced CSCC by ceRNA function and direct recruitment of c-MYC to affect the expression of KTN1, and to regulate EGFR at the post-transcriptional level and translation level, respectively. We will, to this end, to carry out project from the following four aspects: (1) to verify the process of MALAT1, which functioned as ceRNA, to regulate the expression of EGFR at the post-transcriptional level; to study the function of KTN1 as the tumor suppressor gene in CSCC and the function that to regulate the expression of EGFR at the protein expression level, and to explore the molecular mechanism behind; (3) to study the effects of KTN1 changes on the protein expression profile of CSCC by quantitative proteomics analysis. (4) the transplanted tumor model in nude mice and transgenic mouse model were constructed and to verify the above experimental results, in vivo. The project will not only provides potential molecular targets and theoretical basis for the prevention and treatment of CSCC, but also provides new research ideas and theoretical basis for the study of the regulation mechanism of non-coding RNA in epithelial tumorigenesis.