ArticleOncology letters2020
Poly (ADP-ribosylation) of HMGB1 facilitates its acetylation and promotes HMGB1 translocation-associated chemotherapy-induced autophagy in leukaemia cells.
Article in Oncology letters, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 20 citations in OpenAlex.
- High mobility group box 1 and its post-translational modifications: Molecular mechanisms underlying neurodegenerative disease pathogenesis.Neural regeneration research · 2026Article
- HMGB1 Post-Translational Modifications in Epstein-Barr Virus-Associated Nasopharyngeal Carcinoma: Current Evidence, Emerging Mechanistic Concepts, and Unresolved Questions.International journal of molecular sciences · 2026Review
- HMGB1 ubiquitination inhibition and extracellular secretion, mediated by mCancer immunology, immunotherapy : CII · 2026Article
- Deconstructing the RAGE signaling maze: the molecular key to opening a new dimension of ovarian anti-aging.Experimental & molecular medicine · 2026Review
- MicroRNA-181a in acute lymphoblastic leukemia: expression pattern, target genes and its potential as a biomarker.Biochemistry and biophysics reports · 2026Review
- HMGB1 as Double-Edged Regulator of Cancer Therapy: Mechanistic Roles in Chemotherapy Resistance and Immunotherapy Response.OncoTargets and therapy · 2026Review
- HMGB1-BoxA gene therapy in reversing cisplatin resistance in non-small cell lung cancer.PloS one · 2025Article
- Cisplatin Dependent Secretion of Immunomodulatory High Mobility Group Box 1 (HMGB1) Protein from Lung Cancer Cells.Biomolecules · 2023Article
- Autophagy: A Potential Therapeutic Target to Tackle Drug Resistance in Multiple Myeloma.International journal of molecular sciences · 2023Review
- CHIP induces ubiquitination and degradation of HMGB1 to regulate glycolysis in ovarian endometriosis.Cellular and molecular life sciences : CMLS · 2022Article
- The mechanism of HMGB1 secretion and release.Experimental & molecular medicine · 2022Review
- Review
- Extracellular HMGB1 interacts with RAGE and promotes chemoresistance in acute leukemia cells.Cancer cell international · 2021Article
- HMGB1 enhances chemotherapy resistance in multiple myeloma cells by activating the nuclear factor-κB pathway.Experimental and therapeutic medicine · 2021Article
- Role of HMGB1 in Chemotherapy-Induced Peripheral Neuropathy.International journal of molecular sciences · 2020Review
- High mobility group box 1 (HMGB1): a pivotal regulator of hematopoietic malignancies.Journal of hematology & oncology · 2020Review
- Immunological Significance of HMGB1 Post-Translational Modification and Redox Biology.Frontiers in immunology · 2020Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Acute lymphoblastic leukaemia (ALL) is one of the most common and curable types of cancer in paediatric patients. However, chemotherapeutic resistance is a difficult but common obstacle when treating leukaemia in the clinical setting. Studies have demonstrated that drug resistance is partly attributable to autophagy induced by multiple chemotherapeutic agents. As an evolutionarily conserved non-histone chromatin-binding protein, high mobility group box protein 1 (HMGB1) is considered to be an important factor in autophagy, and regulates autophagy at multiple levels via different subcellular localisations. In the present study, it was revealed that chemotherapeutic drugs induced autophagy in leukaemia cells and that translocation of HMGB1 from the nucleus to the cytoplasm is an important molecular event in this process. It was further demonstrated that poly (ADP-ribosylation) of HMGB1 facilitates its acetylation, thereby inducing HMGB1 translocation and ultimately promoting chemotherapy-induced autophagy in leukaemic cells. Targeted HMGB1 translocation may overcome chemotherapy-induced autophagy in leukaemia.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.