ArticleJournal of experimental & clinical cancer research : CR2018
HMGB1 knockdown increases MM cell vulnerability by regulating autophagy and DNA damage repair.
Article in Journal of experimental & clinical cancer research : CR, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 36 citations in OpenAlex.
- HMGB1: A Central Node in Cancer Therapy Resistance.International journal of molecular sciences · 2025Review
- Article
- Single-cell analysis reveals that GFAPCell death & disease · 2025Article
- Mesenchymal stromal cells in bone marrow niche of patients with multiple myeloma: a double-edged sword.Cancer cell international · 2025Review
- Gfi-1 modulates HMGB1-Mediated autophagy to overcome oxaliplatin resistance in colorectal cancer.Heliyon · 2024Article
- The mechanism of high mobility group box-1 protein and its bidirectional regulation in tumors.Biomolecules & biomedicine · 2024Review
- Identification of evolutionary mechanisms of myelomatous effusion by single-cell RNA sequencing.Blood advances · 2023Article
- Mechanisms involved in the HMGB1 modulation of tumor multidrug resistance (Review).International journal of molecular medicine · 2023Article
- Insulin/IGF Axis and the Receptor for Advanced Glycation End Products: Role in Meta-inflammation and Potential in Cancer Therapy.Endocrine reviews · 2023Review
- Autophagy: A Potential Therapeutic Target to Tackle Drug Resistance in Multiple Myeloma.International journal of molecular sciences · 2023Review
- Autophagy-related mechanisms for treatment of multiple myeloma.Cancer drug resistance (Alhambra, Calif.) · 2023Review
- The potential link between Covid-19 and multiple myeloma: A new saga.Immunity, inflammation and disease · 2022Review
- Article
- Deubiquitylase USP12 induces pro-survival autophagy and bortezomib resistance in multiple myeloma by stabilizing HMGB1.Oncogene · 2022Article
- Involvement of Alarmins in the Pathogenesis and Progression of Multiple Myeloma.International journal of molecular sciences · 2021Review
- HMGB1 enhances chemotherapy resistance in multiple myeloma cells by activating the nuclear factor-κB pathway.Experimental and therapeutic medicine · 2021Article
- PIWIL1 Drives Chemoresistance in Multiple Myeloma by Modulating Mitophagy and the Myeloma Stem Cell Population.Frontiers in oncology · 2021Article
- Astragaloside IV and Saponins of Rhizoma Polygonati Cure Cyclophosphamide-Induced Myelosuppression in Lung AdenocarcinomaFrontiers in oncology · 2021Article
- Article
- High mobility group box 1 (HMGB1): a pivotal regulator of hematopoietic malignancies.Journal of hematology & oncology · 2020Review
Corrections and comments
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Authors and funding
12 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundWith the development of novel therapeutic agents, the survival of multiple myeloma (MM) patients has much improved. However, the disease is incurable due to drug resistance. Previous studies have found that high-mobility group box 1 (HMGB1) is involved in inflammation, angiogenesis, DNA damage repair, and cancer invasion, progression, metastasis and drug resistance and that high HMGB1 expression is associated with poor MM prognosis, yet the role and mechanism of HMGB1 in MM remains unclear.
methodsThrough gene expression and Oncomine database analyses, we found that HMGB1 is associated with a poor prognosis in MM patients. RNA interference together with gene array analysis, cell proliferation and apoptosis assays, autophagy detection assays, western blotting, and in vivo xenograft models were employed to evaluate the effect of HMGB1 and the mechanism involved in MM drug resistance.
resultsMM cell lines and primary MM samples were found to express high levels of HMGB1, which was negatively associated with the 3-year survival of MM patients. HMGB1 knockdown in MM cells enhanced the inhibitory effect of chemotherapy with dexamethasone (Dex) via apoptosis induction. Furthermore, downregulation of HMGB1 activated the mTOR pathway, inhibited autophagy and increased DNA damage induced by Dex by modulating expression of related genes. In vivo, xenograft models showed that after Dex treatment, the tumor burden of HMGB1-knockdown mice was decreased compared with that of control mice.
conclusionsOur research shows that HMGB1 participates in autophagy and DNA damage repair and that downregulation of HMGB1 enhances the sensitivity of MM cells to Dex, suggesting that HMGB1 may serve as a target for MM treatment.
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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.