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Updated: Aug 22, 2025

An Integrated Platform for Genome-wide Mapping of Chromatin States Using High-throughput ChIP-sequencing in Tumor Tissues
Published on: April 5, 2018
Targeting Chromatin-Remodeling Factors in Cancer Cells: Promising Molecules in Cancer Therapy
Fang-Lin Zhang1,2,3, Da-Qiang Li1,2,3,4,5,6
1Shanghai Cancer Center and Institutes of Biomedical Sciences, Shanghai Medical College, Fudan University, Shanghai 200032, China.
Abstract:
ATP-dependent chromatin-remodeling complexes can reorganize and remodel chromatin and thereby act as important regulator in various cellular processes. Based on considerable studies over the past two decades, it has been confirmed that the abnormal function of chromatin remodeling plays a pivotal role in genome reprogramming for oncogenesis in cancer development and/or resistance to cancer therapy. Recently, exciting progress has been made in the identification of genetic alteration in the genes encoding the chromatin-remodeling complexes associated with tumorigenesis, as well as in our understanding of chromatin-remodeling mechanisms in cancer biology. Here, we present preclinical evidence explaining the signaling mechanisms involving the chromatin-remodeling misregulation-induced cancer cellular processes, including DNA damage signaling, metastasis, angiogenesis, immune signaling, etc. However, even though the cumulative evidence in this field provides promising emerging molecules for therapeutic explorations in cancer, more research is needed to assess the clinical roles of these genetic cancer targets.
Insights
Chromatin remodeling complexes regulate cell processes. Their abnormal function drives cancer development and therapy resistance, offering potential therapeutic targets.
Area of Science:
- Molecular Biology
- Cancer Biology
- Epigenetics
Background:
- ATP-dependent chromatin-remodeling complexes are crucial regulators of cellular processes.
- Dysfunctional chromatin remodeling is implicated in oncogenesis and cancer therapy resistance.
- Recent advances identify genetic alterations in chromatin remodelers linked to tumorigenesis.
Purpose of the Study:
- To present preclinical evidence on signaling mechanisms of chromatin remodeling misregulation in cancer.
- To elucidate the role of chromatin remodeling in cancer cellular processes like DNA damage, metastasis, angiogenesis, and immune signaling.
Main Methods:
- Review of preclinical evidence and genetic alteration studies.
- Analysis of signaling pathways involved in chromatin remodeling-induced cancer processes.
Main Results:
- Misregulation of chromatin remodeling influences key cancer hallmarks.
- Specific signaling pathways affected include DNA damage, metastasis, angiogenesis, and immune signaling.
- Genetic alterations in chromatin remodeling genes are associated with cancer development.
Conclusions:
- Chromatin remodeling misregulation is a significant driver of cancer cellular processes.
- Emerging therapeutic strategies targeting chromatin remodelers show promise.
- Further clinical research is required to validate these genetic targets for cancer therapy.
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