ArticleInternational journal of clinical and experimental pathology2015
HMGB1-induced autophagy in Schwann cells promotes neuroblastoma proliferation.
Article in International journal of clinical and experimental pathology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 20 citations in OpenAlex.
- TIM-3 blockade enhances ex vivo stimulated allogeneic NK cell therapy for relapsed murine neuroblastoma after hematopoietic cell transplant.Journal for immunotherapy of cancer · 2025Article
- Review
- Review
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- Endogenous HMGB1 regulates GSDME-mediated pyroptosis via ROS/ERK1/2/caspase-3/GSDME signaling in neuroblastoma.American journal of cancer research · 2023Article
- Artificial Tumor Microenvironments in Neuroblastoma.Cancers · 2021Review
- The performance of the alarmin HMGB1 in pediatric diseases: From lab to clinic.Immunity, inflammation and disease · 2021Review
- Article
- Targeting autophagy in neuroblastoma.World journal of pediatric surgery · 2020Review
- Schwann cells shape the neuro-immune environs and control cancer progression.Cancer immunology, immunotherapy : CII · 2019Review
- The progression of HMGB1-induced autophagy in cancer biology.OncoTargets and therapy · 2019Review
- MiR-20a-5p suppresses tumor proliferation by targeting autophagy-related gene 7 in neuroblastoma.Cancer cell international · 2018Article
- Action of HMGB1 on miR-221/222 cluster in neuroblastoma cell lines.Oncology letters · 2016Article
- The role of high mobility group box 1 (HMGB1) in the pathogenesis of kidney diseases.Acta pharmaceutica Sinica. B · 2016Review
- Transcription factor E2-2 inhibits the proliferation of endothelial progenitor cells by suppressing autophagy.International journal of molecular medicine · 2016Article
- HMGB1 induces apoptosis and EMT in association with increased autophagy following H/R injury in cardiomyocytes.International journal of molecular medicine · 2016Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Neuroblastoma inflicts mostly on children, and the pathogenesis remains elusive. Clinical diagnosis and therapeutic approaches are still on the incipient stage, so further understanding of the molecular and cellular mechanisms of the disease is necessary. Inflammation has been commonly regarded as a hallmark in tumorigenesis and development, and we identified a new inflammatory factor, HMGB1, is considerably increased in neuroblastoma. Our study shows that HMGB1 induces autophagy in Schwann cells through activation of TLR4, and knockdown of TLR4 obviates the HMGB1-induced autophagy. The HMGB1-induced autophagy is through classical pathway, as deficiency of Beclin 1 deprived autophagy in Schwann cells. Coculture of neuroblastoma with Schwann cells pretreated with HMGB1 promoted the proliferation of neuroblastoma cells, and if Beclin 1 is knocked down in Schwann cells, no promotion effects is observed. Taken together, our study demonstrates that HMGB1-induced autophagy in Schwann cells contributes to neuroblastoma cell proliferation, thus providing a potential therapeutic approach on neuroblastoma development.
Indexed as
Identifiers
25755740PMC4348936W2255429211What OpenQuestion holds
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.