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CDCA7 Promotes Neuroblastoma Proliferation via Regulating the Cell Cycle
Wen Yuan1, Xiaoxing Huang2, Renwei Luo3
1Department of Laboratory Medicine, Wuhan Children's Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei 430016, China.
Iranian Journal of Biotechnology
|May 18, 2026
Summary
Cell division cycle-associated 7 (CDCA7) is overexpressed in neuroblastoma (NB) and linked to poor survival. Silencing CDCA7 inhibits NB cell proliferation by causing G1 cell cycle arrest and reducing CDK6 expression.
Area of Science:
- Oncology
- Molecular Biology
- Cancer Research
Background:
- Cell division cycle-associated 7 (CDCA7) is implicated in various cancers, but its role in neuroblastoma (NB) remains undefined.
- Understanding CDCA7's function in NB is crucial for developing targeted therapies.
Purpose of the Study:
- To investigate the expression, clinical significance, and biological functions of CDCA7 in neuroblastoma.
- To elucidate the molecular mechanisms by which CDCA7 regulates NB cell proliferation and cell cycle progression.
Main Methods:
- Analysis of NB datasets to assess CDCA7 expression and correlation with clinical features.
- In vitro studies involving CDCA7 knockdown using shRNA, cell proliferation assays (CCK8), cell cycle analysis (flow cytometry), and molecular analysis (qPCR, Western blotting).
- Evaluation of CDCA7's association with immune cell infiltration.
Main Results:
- CDCA7 is highly expressed in NB tissues and cell lines, with elevated levels in MYCN-amplified NB and advanced stages.
- High CDCA7 expression correlates with poor overall survival (OS) and event-free survival (EFS) in NB patients.
- CDCA7 knockdown suppressed proliferation, induced G1 cell cycle arrest, and decreased CDK6 expression, while also showing associations with immune cell infiltration (B cells, CD4+ T cells, macrophages).
Conclusions:
- CDCA7 serves as a potential prognostic biomarker for neuroblastoma.
- CDCA7 inhibition results in G1 cell cycle arrest and reduced CDK6 expression, thereby inhibiting NB cell proliferation.
- CDCA7 influences the tumor microenvironment through its association with immune cell infiltration.
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