ArticleComputational and structural biotechnology journal2021
Synergistic alterations in the multilevel chromatin structure anchor dysregulated genes in small cell lung cancer.
Article in Computational and structural biotechnology journal, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 10 citations in OpenAlex.
- HMGA2 interacts with KAT6A to regulate MMPs chromatin architecture and promote triple-negative breast cancer metastasis.Frontiers in immunology · 2025Article
- Advancing therapeutic target discovery in pulmonary diseases: evolution and application of space exploration technologies.Frontiers in cell and developmental biology · 2025Review
- 3D genomic organization in cancers.Quantitative biology (Beijing, China) · 2023Review
- A global high-density chromatin interaction network reveals functional long-range and trans-chromosomal relationships.Genome biology · 2022Article
- Multilevel view on chromatin architecture alterations in cancer.Frontiers in genetics · 2022Review
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Authors and funding
15 authors at 3 institutions in 1 country.
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Abstract
Small cell lung cancer (SCLC) is an aggressive form of lung cancer that uniquely changes the chromosomal structure, although the basis of aberrant gene expression in SCLC remains largely unclear. Topologically associated domains (TADs) are structural and functional units of the human genome. Genetic and epigenetic alterations in the cancer genome can lead to the disruption of TAD boundaries and may cause gene dysregulation. To understand the potential regulatory role of this process in SCLC, we developed the TAD boundary alteration-related gene identification in tumors (TARGET) computational framework, which enables the systematic identification of candidate dysregulated genes associated with altered TAD boundaries. Using TARGET to compare gene expression profiles between SCLC and normal human lung fibroblast cell lines, we identified >100 genes in this category, of which 24 were further verified in samples from patients with SCLC using NanoString. The analysis revealed synergistic chromatin structure alteration at the A/B compartment and TAD boundary levels that underlies aberrant gene expression in SCLC. TARGET is a novel and powerful tool that can be used to explore the relationship of chromatin structure alteration to gene dysregulation related to SCLC tumorigenesis, progression, and prognosis.
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