SYT7作为一种癌基因和潜在的治疗靶点，在头颈部鳞状细胞癌中受ΔNp63α调控。
SYT7 acts as an oncogene and a potential therapeutic target and was regulated by ΔNp63α in HNSCC.
作者信息
Fu You, Tian Guocai, Zhang Zhiyuan, Yang Xiao
机构信息
Department of Oral and Maxillofacial-Head Neck Oncology, Shanghai Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, College of Stomatology, National Center for Stomatology, National Clinical Research Center for Oral Diseases, Shanghai Jiao Tong University, 639 Zhizaoju Road, Shanghai, 200011, People's Republic of China.
Shanghai Key Laboratory of Stomatology, Research Unit of Oral and Maxillofacial Regenerative Medicine, Chinese Academy of Medical Sciences, Beijing, China.
出版信息
Cancer Cell Int. 2021 Dec 20;21(1):696. doi: 10.1186/s12935-021-02394-w.
BACKGROUND
Head and neck squamous cell carcinoma (HNSCC) are one of the most common types of head and neck cancer, and it is urgent to find effective treatment for advanced patients. Exploring developing and progressing mechanisms of HNSCC could provide a theoretical basis to find new therapeutic targets.
METHODS
In our research, we performed a whole-gene expression profile microarray analysis to identify differential expression genes between squamous cell carcinoma cells and ΔNp63 alpha (ΔNp63α) knockdown cells. As a result, an important gene Synaptotagmin VII (SYT7) was screened out.
RESULTS
SYT7 knockdown affected the proliferation, apoptosis and cell cycle of squamous cell carcinoma cells. The rescue experiment in vitro with ΔNp63α and SYT7 double knockdown resulted in partial reversion of ΔNp63α-induced phenotypes. This was also confirmed by experiments in vivo.
CONCLUSIONS
Taken together, we found that ΔNp63α could inhibit the occurrence and progression of HNSCC throughout downregulating the expression of SYT7. Therefore, SYT7/ΔNp63α axis could be a potential therapeutic target for clinical treatment of HNSCC.
背景
头颈部鳞状细胞癌（HNSCC）是头颈部最常见的癌症类型之一，为晚期患者寻找有效的治疗方法迫在眉睫。探索HNSCC的发生发展机制可为寻找新的治疗靶点提供理论依据。
方法
在我们的研究中，我们进行了全基因表达谱微阵列分析，以鉴定鳞状细胞癌细胞和ΔNp63α敲低细胞之间的差异表达基因。结果，筛选出一个重要基因突触结合蛋白VII（SYT7）。
结果
SYT7敲低影响鳞状细胞癌细胞的增殖、凋亡和细胞周期。在体外进行的ΔNp63α和SYT7双敲低的挽救实验导致ΔNp63α诱导的表型部分逆转。体内实验也证实了这一点。
结论
综上所述，我们发现ΔNp63α可通过下调SYT7的表达来抑制HNSCC的发生和发展。因此，SYT7/ΔNp63α轴可能是HNSCC临床治疗的潜在治疗靶点。
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