Related Experiment Video
Updated: Jul 16, 2026

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Repressing Gene Transcription by Redirecting Cellular Machinery with Chemical Epigenetic Modifiers
Published on: September 20, 2018
H3K4me3 and H3K27ac Promote ccRCC Proliferation Through the CDC6-EXOSC5 Axis
Peng Cui1,2, Juan Luo1, Ping Zhang3
1Precision Medicine Institute, Peking University Shenzhen Hospital, Shenzhen 518036, China.
International Journal of Molecular Sciences
|July 15, 2026
Summary
CDC6, a gene linked to cancer, is highly overexpressed in clear cell renal cell carcinoma (ccRCC). Its regulation by epigenetic modifications like histone methylation drives tumor growth and progression.
Area of Science:
- Oncology
- Molecular Biology
- Epigenetics
Background:
- Renal cell carcinoma (RCC), particularly clear cell RCC (ccRCC), is a major cause of cancer mortality.
- CDC6 is an oncogene implicated in tumor grading and prognosis.
Purpose of the Study:
- To investigate the role of CDC6 in ccRCC pathogenesis.
- To elucidate the regulatory mechanisms of CDC6 expression in ccRCC.
- To explore the diagnostic and prognostic relevance of the SETD1A-CDC6-EXOSC5 axis in ccRCC.
Main Methods:
- Analysis of The Cancer Genome Atlas (TCGA) data for gene expression.
- Cellular proliferation assays (CCK-8 and EdU incorporation).
- Investigation of epigenetic modifications (histone acetylation and methylation) and their impact on CDC6 transcription.
Main Results:
- CDC6 is significantly overexpressed in ccRCC tissues compared to normal tissues (97.22%).
- CDC6 knockdown suppresses ccRCC cell viability and proliferation.
- CDC6 transcription is epigenetically regulated by histone H3K4 trimethylation, potentially mediated by SETD1A.
- The SETD1A-CDC6-EXOSC5 axis is implicated in ccRCC development.
Conclusions:
- Increased CDC6 expression, driven by epigenetic mechanisms, promotes ccRCC progression.
- The SETD1A-CDC6-EXOSC5 axis represents a potential therapeutic target and biomarker for ccRCC.
- Findings provide insights into ccRCC pathogenesis and support new diagnostic strategies.
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