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SNAP23 suppresses cervical cancer progression via modulating the cell cycle
Biqing Zhu1, Quanli Zhang2, Yaqin Wu1
1Department of Radiation Oncology, Jiangsu Cancer Hospital, Jiangsu Institute of Cancer Research, The Affiliated Cancer Hospital of Nanjing Medical University, Nanjing, 210009, PR China; Jiangsu Key Laboratory of Molecular and Translational Cancer Research, Jiangsu Cancer Hospital, Jiangsu Institute of Cancer Research, The Affiliated Cancer Hospital of Nanjing Medical University, Nanjing, 210009, PR China.
Gene
|June 18, 2018
Summary
SNAP23 acts as a tumor suppressor in cervical cancer (CC), inhibiting progression and inducing cell cycle arrest. Its downregulation correlates with advanced disease, suggesting therapeutic potential.
Area of Science:
- Oncology
- Molecular Biology
- Gynecologic Oncology
Background:
- Cervical cancer (CC) is a prevalent gynecologic malignancy with poor patient outcomes.
- Identifying novel tumor suppressor genes is crucial for developing effective CC therapies.
Purpose of the Study:
- To investigate the role of SNAP23 as a potential tumor suppressor in cervical cancer.
- To elucidate the molecular mechanisms underlying SNAP23's function in CC progression.
Main Methods:
- Quantitative real-time PCR (qRT-PCR), Western blot, and immunohistochemistry (IHC) were used to assess SNAP23 expression.
- In vitro experiments involved SNAP23 knockdown (siRNA) and overexpression (plasmid).
- In vivo studies utilized xenograft nude mouse models to evaluate tumor growth.
Main Results:
- SNAP23 expression was significantly downregulated in CC tissues and negatively correlated with advanced clinical characteristics.
- Overexpression of SNAP23 suppressed CC cell malignant phenotypes, while knockdown promoted progression.
- Flow cytometry revealed that SNAP23 induces G2/M cell cycle arrest, suppressing tumor growth in vivo.
Conclusions:
- SNAP23 functions as a tumor suppressor in cervical cancer.
- SNAP23 suppresses CC progression by inducing G2/M cell cycle arrest.
- This is achieved through the upregulation of p21cip1 and downregulation of CyclinB1.
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