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SYT7 (synaptotagmin 7) promotes cervical squamous cell carcinoma
Jinbing Huang1, Wensheng Xu1, Qiaoqiao Huang1
1Department of Gynecology and Obstetrics, The First Affiliated Hospital of Guangxi Medical University, 6 Shuangyong Road, Nanning, Guangxi, China.
Heliyon
|February 5, 2024
Summary
Synaptotagmin 7 (SYT7) promotes cervical squamous cell carcinoma (CESC) growth. Silencing SYT7 inhibited tumor cell proliferation, migration, and invasion, offering a potential therapeutic target for CESC.
Area of Science:
- Oncology
- Molecular Biology
- Cell Biology
Background:
- Cervical squamous cell carcinoma (CESC) is a major cause of cancer mortality worldwide.
- The specific role of synaptotagmin 7 (SYT7) in CESC pathogenesis is not well understood.
Purpose of the Study:
- To investigate the expression and function of SYT7 in CESC.
- To determine the potential of SYT7 as a therapeutic target for CESC.
Main Methods:
- Immunohistochemistry was used to assess SYT7 expression in CESC tissues.
- SYT7 knockdown cell line models (HeLa, SiHa) were created using lentiviral shRNA.
- In vitro functional assays (proliferation, colony formation, apoptosis, migration, invasion) and in vivo xenograft models were employed.
Main Results:
- SYT7 expression was significantly elevated in CESC tissues compared to normal tissues.
- SYT7 knockdown suppressed cell proliferation, colony formation, migration, and invasion, while enhancing apoptosis.
- In vivo, SYT7 knockdown inhibited tumor growth and tumorigenic potential.
- SYT7 depletion altered the expression of key apoptosis and signaling pathway genes.
Conclusions:
- SYT7 plays a tumor-promoting role in CESC.
- Targeting SYT7 may represent a novel therapeutic strategy for cervical squamous cell carcinoma.
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