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CHD4/NuRD complex regulates complement gene expression and correlates with CD8 T cell infiltration in human
Simin Shao1, Haowei Cao1, Zhongkun Wang1
1Jiangsu Key Laboratory of Brain Disease and Bioinformation, Research Center for Biochemistry and Molecular Biology, Xuzhou Medical University, Xuzhou, China.
The Nucleosome Remodeling and Deacetylation (NuRD) complex, particularly CHD4, promotes hepatocellular carcinoma (HCC) by driving cancer progression and regulating immune cell infiltration. Its overexpression correlates with poor prognosis in HCC patients.
Area of Science:
- Molecular Biology
- Cancer Research
- Epigenetics
Background:
- The Nucleosome Remodeling and Deacetylation (NuRD) complex regulates gene transcription by altering chromatin accessibility.
- While individual NuRD subunits are linked to various cancers, its comprehensive role in hepatocellular carcinoma (HCC) remains unclear.
- The NuRD complex has not been previously investigated as a whole in cancer contexts.
Purpose of the Study:
- To investigate the expression and prognostic value of the NuRD complex in HCC.
- To elucidate the functional role of the CHD4/NuRD complex in HCC progression and the tumor microenvironment.
Main Methods:
- Analysis of NuRD complex expression using TCGA RNA-seq data in HCC.
- Functional studies involving CHD4 knockdown in HCC cell lines.
- Bioinformatic analysis of NuRD expression correlation with immune infiltration.
Main Results:
- Nine of 14 examined NuRD subunits were overexpressed in HCC, correlating with cancer progression.
- CHD4 knockdown inhibited HCC cell proliferation, migration, invasion, and colony formation, while promoting apoptosis.
- The CHD4/NuRD complex was found to regulate complement gene expression and inversely correlate with CD8 T cell and DC cell infiltration.
Conclusions:
- The CHD4/NuRD complex plays a significant oncogenic role in human HCC.
- This complex regulates complement gene expression and impacts the HCC immune microenvironment.
- NuRD complex expression serves as a potential prognostic marker and therapeutic target in HCC.
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