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SYT7 acts as an oncogene and a potential therapeutic target and was regulated by ΔNp63α in HNSCC
You Fu1,2, Guocai Tian1,2, Zhiyuan Zhang3,4
1Department 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.
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.
Insights
Head and neck squamous cell carcinoma (HNSCC) progression is linked to Synaptotagmin VII (SYT7) expression. Targeting the SYT7/ΔNp63α axis offers a potential new therapy for HNSCC patients.
Area of Science:
- Oncology
- Molecular Biology
- Cancer Research
Background:
- Head and neck squamous cell carcinoma (HNSCC) is a prevalent cancer requiring novel treatments for advanced stages.
- Understanding HNSCC development mechanisms is crucial for identifying new therapeutic targets.
Purpose of the Study:
- To investigate the role of Synaptotagmin VII (SYT7) in HNSCC progression.
- To explore the relationship between ΔNp63 alpha (ΔNp63α) and SYT7 in HNSCC.
Main Methods:
- Whole-gene expression profile microarray analysis was conducted to identify differentially expressed genes.
- Gene knockdown experiments (ΔNp63α and SYT7) were performed in vitro and in vivo.
Main Results:
- Synaptotagmin VII (SYT7) was identified as a key gene differentially expressed in HNSCC cells.
- SYT7 knockdown significantly impacted HNSCC cell proliferation, apoptosis, and cell cycle.
- Rescue experiments demonstrated that SYT7 downregulation partially reversed ΔNp63α-induced HNSCC phenotypes.
Conclusions:
- ΔNp63α inhibits HNSCC occurrence and progression by downregulating SYT7 expression.
- The SYT7/ΔNp63α axis represents a promising therapeutic target for HNSCC clinical treatment.
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