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Development of Compendium for Esophageal Squamous Cell Carcinoma
Published on: April 12, 2024
Low expression of cyclinH and cyclin-dependent kinase 7 can decrease the proliferation of human esophageal squamous
Jianguo Zhang1, Xiaojing Yang, Yuchan Wang
1Department of Immunology, Medical College, Nantong University, 19 Qi-Xiu Road, Nantong 226001, Jiangsu, People's Republic of China.
Digestive Diseases and Sciences
|March 5, 2013
Summary
Cyclin H (CCNH) and Cyclin-Dependent Kinase 7 (CDK7) are elevated in esophageal squamous cell carcinoma (ESCC), correlating with poor prognosis and impacting chemotherapy effectiveness.
Area of Science:
- Oncology
- Molecular Biology
- Cancer Research
Background:
- Elevated cyclin H (CCNH) and cyclin-dependent kinase 7 (CDK7) expression are linked to poor prognosis in various human cancers.
- Understanding the role of CCNH and CDK7 in esophageal squamous cell carcinoma (ESCC) is crucial for developing targeted therapies.
Purpose of the Study:
- To investigate the expression levels of CCNH and CDK7 in human ESCC tissues.
- To determine the effect of chemotherapy, specifically cisplatin, on CCNH and CDK7 expression in ESCC.
- To explore the functional role of CCNH and CDK7 in ESCC cell cycle progression and cisplatin resistance.
Main Methods:
- Western blotting and immunohistochemistry were employed to quantify CCNH and CDK7 protein levels in 98 ESCC patient samples and adjacent normal tissues.
- Cell Counting Kit-8 and flow cytometry were utilized to assess the impact of cisplatin and CCNH/CDK7 interference on ESCC cell proliferation and cell cycle dynamics.
- TE1 cell line was used to study the effects of CCNH and CDK7 overexpression on cisplatin sensitivity.
Main Results:
- CCNH and CDK7 protein levels were significantly higher in ESCC tissues compared to normal tissues.
- Increased expression of CCNH and CDK7 was strongly associated with unfavorable clinicopathologic features and reduced overall survival in ESCC patients (P < 0.001).
- Cisplatin treatment or interference with CCNH/CDK7 function resulted in decreased ESCC cell growth, and CCNH/CDK7 overexpression conferred resistance to cisplatin.
Conclusions:
- CCNH and CDK7 play a significant role in the tumorigenesis and progression of ESCC.
- The expression of CCNH and CDK7 influences the response of ESCC tumors to chemotherapy, suggesting their potential as therapeutic targets.
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