SYT7 acts as an oncogene and a potential therapeutic target and was regulated by ΔNp63α in HNSCC.
SYT7 acts as an oncogene and a potential therapeutic target and was regulated by ΔNp63α in HNSCC.
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SYT7 作为癌基因和潜在的治疗靶点，在 HNSCC 中受 ΔNp63α 调节
DOI：
10.1186/s12935-021-02394-w
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发表时间：
2021-12-20
影响因子：
5.8
通讯作者：
Yang X
中科院分区：
文献类型：
--
作者：
Fu Y;Tian G;Zhang Z;Yang X
头颈部鳞状细胞癌是最常见的头颈部恶性肿瘤之一，对晚期患者寻找有效的治疗方法是当务之急。探讨HNSCC的发生、发展机制，为寻找新的治疗靶点提供理论依据。在我们的研究中，我们进行了全基因表达谱芯片分析，以确定鳞状细胞癌细胞和Δ Np 63 α（Δ Np 63 α）敲除细胞之间的差异表达基因。结果筛选出一个重要的基因Synaptotagmin VII（SYT 7）。SYT 7基因敲除影响鳞状细胞癌细胞的增殖、凋亡和细胞周期。在体外用Δ Np 63 α和SYT 7双敲低进行的拯救实验导致Δ Np 63 α诱导的表型的部分逆转。这一点也得到了体内实验的证实。综上所述，我们发现Δ Np 63 α可以通过下调SYT 7的表达来抑制HNSCC的发生和发展。因此，SYT 7/Δ Np 63 α轴可能成为HNSCC临床治疗的潜在靶点。在线版本包含补充材料，可通过10.1186/s12935-021-02394-w获得。
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. 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. 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. 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. The online version contains supplementary material available at 10.1186/s12935-021-02394-w.
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