ArticleScientific reports2025
The role of Box A of HMGB1 in producing γH2AX associated DNA breaks in lung cancer.
Article in Scientific reports, 2025. 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.
- Exploratory Analysis of HMGB1 Genetic Variants and Their Potential Association with Lung Cancer Susceptibility and Chemotherapy Response in a Chinese Population.Human heredity · 2026Article
- HMGB1: A Central Node in Cancer Therapy Resistance.International journal of molecular sciences · 2025Review
- HMGB1 as a Key Mediator in Malignant Mesothelioma and a Potential Target for Asbestos-Related Cancer Therapy.Toxics · 2025Article
- HMGB1-BoxA gene therapy in reversing cisplatin resistance in non-small cell lung cancer.PloS one · 2025Article
- Long-term Safety Pharmacology and Musculoskeletal Changes of HMGB1 Box A Gene Therapy in Middle-aged Monkeys.In vivo (Athens, Greece)Article
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Authors and funding
3 authors.
Funding
Abstract
An ideal chemotherapeutic agent damages DNA, specifically in cancer cells, without harming normal cells. Recently, we used Box A of HMGB1 plasmid as molecular scissors to produce DNA gaps in normal cells. The DNA gap relieves DNA tension and increases DNA strength, preventing DNA double-strand breaks (DSBs). Since the formation of HMGB1-produced DNA gaps in cancers may differ from normal cells, the outcome of introducing Box A into cancer cells may be different. We demonstrated that in lung cancer cells, γH2AX foci and histone modification associating DSBs were produced by Box A. We transfected Box A plasmid into lung cancer cell lines to overexpress Box A and evaluated the expression levels of γH2AX foci and other DNA damage response (DDR) signaling cascade markers, including ATM, ATR, and p53. Then, we demonstrated the downstream effects of DSBs on lung cancer, lowering cell proliferation, decreasing cell migration, and promoting apoptosis. Thus, Box A in lung cancer promoted the opposite outcome to normal cells by breaking cancer DNA.
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