ArticleInternational journal of molecular medicine2017
EWS-FLI1 positively regulates autophagy by increasing ATG4B expression in Ewing sarcoma cells.
Article in International journal of molecular medicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 22 citations in OpenAlex.
- Autophagy impairs the sensitivity of Ewing sarcoma cells to PARP inhibitors.Cancer chemotherapy and pharmacology · 2026Article
- Targeting autophagy and metabolism for ewing sarcoma.Molecular biology reports · 2025Review
- Prognostic value ofHeliyon · 2023Article
- Latest developments in the pathobiology of Ewing sarcoma.Journal of bone oncology · 2022Review
- The prognostic value of autophagy related genes with potential protective function in Ewing sarcoma.BMC bioinformatics · 2022Article
- The Controversial Role of Autophagy in Ewing Sarcoma Pathogenesis-Current Treatment Options.Biomolecules · 2021Review
- TRIM3 Negatively Regulates Autophagy Through Promoting Degradation of Beclin1 in Ewing Sarcoma Cells.OncoTargets and therapy · 2019Article
- A review of soft-tissue sarcomas: translation of biological advances into treatment measures.Cancer management and research · 2018Review
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ewing sarcoma (ES) is the most common malignant bone tumor in children and young adults. It is characterized by chromosomal translocations fusing the EWS gene with an ETS oncogene, most frequently FLI1. In the present study, the authors aimed to investigate the function of EWS-FLI1 in autophagy in ES cells, and identified that EWS-FLI1 positively regulates autophagy in ES cells. ATG4B expression was observed markedly upregulated by EWS-FLI1 overexpression, and silencing of ATG4B dramatically inhibits autophagy in ES cells. Furthermore, apoptosis was inhibited in ATG4B overexpressed ES cells, and ATG4B-potentiated autophagy is required for ES cells survival. Taken together, the authors demonstrated the role of EWS-FLI1 and ATG4B in autophagy in ES cells, and suggested EWS-FLI1 and ATG4B as potential therapeutic targets for ES.
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