ArticleCell proliferation2021
Loss of SMARCB1 promotes autophagy and facilitates tumour progression in chordoma by transcriptionally activating ATG5.
Article in Cell proliferation, 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, 13 citations in OpenAlex.
- Reoviruses hijack the SMARCB1-MYC transcriptional regulation complex to activate autophagy for persistent viral infection in leafhopper vector.PLoS pathogens · 2025Article
- Animal model considerations for chordoma research: reproducing the tumor microenvironmentFrontiers in oncology · 2024Review
- SMARCB1/INI1 loss in skull base conventional chordomas: a clinicopathological and molecular analysis.Frontiers in oncology · 2023Article
- The critical roles of lnc-GLYATL2-2/PD-L1 axis in immune microenvironment and the clinical value of intracranial chordomas.American journal of cancer research · 2023Article
- MoSnf5 Regulates Fungal Virulence, Growth, and Conidiation inJournal of fungi (Basel, Switzerland) · 2022Article
- Factors associated with artificial airway retention after skull base chordoma resection: A retrospective cohort study.Frontiers in neurology · 2022Article
- Loss of SMARCB1 promotes autophagy and facilitates tumour progression in chordoma by transcriptionally activating ATG5.Cell proliferation · 2021Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
objectivesSWI/SNF-related matrix-associated actin-dependent regulator of chromatin subfamily B member 1 (SMARCB1) loss is associated with a poor prognosis in chordoma, while the mechanism remains largely unclear. Here, we aim to explore the function and regulatory mechanisms of SMARCB1 in chordoma. MATERIALS AND
methodsThe effect of SMARCB1 on chordoma cells was investigated in vitro and in vivo. Chromatin immunoprecipitation (ChIP) sequencing was used to investigate the mechanisms of SMARCB1 in chordoma. The association between SMARCB1 and autophagy was validated by Western blot, immunofluorescence and transmission electron microscopy. In addition, the ATG5 expression in chordoma tissue was assessed using immunohistochemistry and correlated with patient survival.
resultsSMARCB1 inhibited the malignant phenotype of chordoma cells in vitro and in vivo, supporting a tumour suppressor role of SMARCB1 in chordoma. ATG5-mediated autophagy was identified as a potential downstream pathway of SMARCB1. Mechanistically, SMARCB1 bound directly to the ATG5 promoter and epigenetically inhibited its transcription, which decreased ATG5 expression and impaired autophagy. Additionally, autophagy inhibitor chloroquine had a potential anti-cancer effect on chordoma cells in vitro. Moreover, high ATG5 expression was observed in recurrent chordoma patients, which independently correlated with adverse outcomes.
conclusionsTaken together, our results revealed that the SMARCB1/ATG5 axis is a promising therapeutic target for chordoma and autophagy inhibitors may be effective agents for chordoma treatment.
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