ArticleCancer cell international2021
Circ_0001721 enhances doxorubicin resistance and promotes tumorigenesis in osteosarcoma through miR-758/TCF4 axis.
Article in Cancer cell international, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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Who cites it
7 citing papers in PubMed, 17 citations in OpenAlex.
- Circular RNAs in osteosarcoma: mechanistic insights, autophagy regulation, and potential therapeutic strategies.Cancer cell international · 2026Review
- Identification and characterization of mitochondrial autophagy-related genes in osteosarcoma and predicting clinical prognosis.Scientific reports · 2025Article
- Research progress of circRNAs in bone-related diseases.Frontiers in oncology · 2025Review
- Chitosan-based nanoscale systems for doxorubicin delivery: Exploring biomedical application in cancer therapy.Bioengineering & translational medicine · 2023Review
- Circular RNA_ANKIB1 accelerates chemo-resistance of osteosarcoma via binding microRNA-26b-5p and modulating enhancer of zeste homolog 2.Bioengineered · 2022Article
- Non-coding RNAs as potential biomarkers in osteosarcoma.Frontiers in genetics · 2022Review
- The Role of Circular RNAs in the Drug Resistance of Cancers.Frontiers in oncology · 2021Review
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
backgroundOsteosarcoma (OS) is a common type of bone malignancy that often occurs in children and adolescents. Chemoresistance is a huge barrier to cancer therapy. This study aimed to investigate the role and potential mechanism of circ_0001721 in doxorubicin (DXR) resistance and OS development.
methodsThe levels of circ_0001721, miR-758 and transcription factor 4 (TCF4) were detected by quantitative real-time polymerase chain reaction or western blot assay. Cell Counting Kit-8 (CCK-8) assay was used to calculate the half inhibition concentration (IC
resultsCirc_0001721 and TCF4 were upregulated, whereas miR-758 was down-regulated in DXR-resistant OS tissues and cells. Circ_0001721 silence reduced DXR resistance of KHOS/DXR and MG63/DXR cells. Circ_0001721 regulated DXR resistance via sponging miR-758. Moreover, miR-758 modulated DXR resistance by targeting TCF4. Besides, circ_0001721 knockdown inhibited tumor growth in vivo.
conclusionCirc_0001721 potentiated DXR resistance and facilitated the progression of OS by regulating miR-758/TCF4 axis, which provides promising therapeutic targets for OS treatment.
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Registered trials
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