ArticleInternational journal of clinical and experimental pathology2017
Upregulation of ATG4A promotes osteosarcoma cell epithelial-to-mesenchymal transition through the Notch signaling pathway.
Article in International journal of clinical and experimental pathology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
8 citing papers in PubMed, 10 citations in OpenAlex.
- Epithelial-Mesenchymal Transition in Osteosarcoma as a Key Driver of Pulmonary Metastasis.Cancers · 2025Review
- Disclosure of Potential Therapeutic Targets in Plumbagin for Treating Osteosarcoma.Biomedical engineering and computational biology · 2025Article
- Review
- Self-Renewal and Pluripotency in Osteosarcoma Stem Cells' Chemoresistance: Notch, Hedgehog, and Wnt/β-Catenin Interplay with Embryonic Markers.International journal of molecular sciences · 2023Review
- Knockdown of ATG4A inhibits breast cancer progression and promotes tamoxifen chemosensitivity by suppressing autophagy.Molecular medicine reports · 2022Article
- In Silico Analysis Identifies Upregulated lncRNA DLGAP1-AS1 Which Is Correlated to Poor Prognosis and Promotes Cell Proliferation in Glioblastoma.Computational and mathematical methods in medicine · 2022Article
- Review
- Prognostic Signature of Osteosarcoma Based on 14 Autophagy-Related Genes.Pathology oncology research : POR · 2021Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Osteosarcoma is a malignant tumor in children and adolescents. Previous studies showed that ATG4A is an autophagy-related gene involved in cancers. In this study, we aimed to identify the biological role of ATG4A in osteosarcoma. The expression levels of ATG4A were analyzed in osteosarcoma tissues by using reverse transcription-quantitative polymerase chain reaction (qRT-PCR) and western blotting. ATG4A was knocked-down or overexpressed in SAOS2 and HOS cell lines by transfection. Cell counting kit-8 (CCK-8) and clone formation assay were used to assess the effects of ATG4A on cell proliferation. Wound healing and Transwell assays were performed to evaluate the effects of ATG4A on cell migration and invasion, respectively. Epithelial-mesenchymal transition (EMT) markers and Notch signaling pathway targeting molecules were examined by western blotting. The results indicated that ATG4A was up-regulated in osteosarcoma tissues. In SAOS2 cells, knockdown of ATG4A inhibited the proliferation, migration and invasion, up-regulated the expression of E-cadherin and down-regulated the expression of vimentin, Notch1 and Hes1. In HOS cells, overexpression of ATG4A promoted the proliferation, migration and invasion, up-regulated the expression of vimentin, Notch1 and Hes1 and down-regulated the expression of E-cadherin. In conclusion, these findings demonstrate that ATG4A is up-regulated in osteosarcoma tissues. In osteosarcoma cells, ATG4A promotes the EMT process partly by the Notch signaling pathway. These results suggest that ATG4A might represent a potential therapeutic target for patients with osteosarcoma.
Indexed as
Identifiers
31966649PMC6965260W3026624482What 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.