ArticleOncology letters2021
HMGB1 knockdown increases the radiosensitivity of esophageal squamous cell carcinoma by regulating the expression of molecules involved in DNA repair.
Article in Oncology letters, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 6 citations in OpenAlex.
- Review
- HMGB1 promotes radiotherapy resistance in human cervical cancer HeLa cells through regulating the AMPK/mTOR signaling.World journal of surgical oncology · 2026Article
- HMGB1 reduce DNA damage by binding KU70 to activate NHEJ pathway in colorectal cancer cells after radiation.PloS one · 2026Article
- Glycyrrhizin ameliorates colorectal cancer progression by regulating NHEJ pathway through inhibiting HMGB1-induced DNA damage response.Scientific reports · 2024Article
- Mechanisms of radiotherapy resistance and radiosensitization strategies for esophageal squamous cell carcinoma.Molecular cancer · 2023Review
- HMGB1 induces radioresistance through PI3K/AKT/ATM pathway in esophageal squamous cell carcinoma.Molecular biology reports · 2022Article
- A novel immune-related radioresistant lncRNAs signature based model for risk stratification and prognosis prediction in esophageal squamous cell carcinoma.Frontiers in genetics · 2022Article
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Radiotherapy is an effective therapeutic strategy in esophageal squamous cell carcinoma (ESCC). However, acquired radioresistance of cancer cells leads to radiotherapy failure. The present study aimed to investigate the mechanisms of the effect of high mobility group box 1 (HMGB1) on the radiation sensitivity of ESCC. Small interfering RNA (si) transfection was used to generate three groups of TE-1 cells (TE-1, negative control and TE-1+siHMGB1), and the protein expression levels of HMGB1 in TE-1 cells were detected by western blotting. These groups of TE-1 cells were irradiated with different doses (0, 2, 4, 6 and 8 Gy) of X-rays after transfection. Subsequently, the viability of TE-1 cells was detected using an MTT assay, and the survival fraction of TE-1 cells was observed using a colony formation assay. The apoptotic rate, reactive oxygen species (ROS) content and levels of phosphorylated (p)-histone H2AX at S139 (p-γH2AX) of the cells were detected by flow cytometry. The alterations in mRNA expression levels of nicotinamide adenine nucleotide phosphate oxidase (NOX)1 and NOX5 were detected by reverse transcription-quantitative PCR, while the changes in protein levels of caspase-3, poly(ADP-ribose) polymerase, p-p38, p-ERK1/2 and p-JNK were detected by western blotting. The results revealed that HMGB1 knockdown significantly decreased cell viability, and the apoptosis rate of TE-1 cells transfected with siHMGB1 combined with radiation treatment was increased compared with that in cells with either siHMGB1 transfection or radiation treatment alone. HMGB1 knockdown increased nicotinamide adenine nucleotide phosphate oxidase-mediated ROS production and induced DNA damage via the MAPK signaling pathway, which may promote apoptosis and radiosensitivity after radiation in TE-1 cells. In conclusion, targeting HMGB1 may represent a promising strategy to increase the efficacy of radiation therapy for ESCC.
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