ArticleNeurochemical research2021
Gain of circBRAF Represses Glioma Progression by Regulating miR-1290/FBXW7 Axis.
Article in Neurochemical research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 9 citations in OpenAlex.
- Molecular mechanism ofTranslational cancer research · 2026Article
- Therapeutic Potential of Circular RNAs as Targets for Cancer Treatment.Advanced pharmaceutical bulletin · 2025Review
- Emerging role and clinical applications of circular RNAs in human diseases.Functional & integrative genomics · 2025Review
- Circular RNAs and Cancers.Advances in experimental medicine and biology · 2025Review
- The landscape of circRNAs in gliomas temozolomide resistance: Insights into molecular pathways.Non-coding RNA research · 2024Review
- Circular RNAs in glioma: Molecular functions and pathological implications.Non-coding RNA research · 2024Review
- Roles of circular RNAs in regulating the development of glioma.Journal of cancer research and clinical oncology · 2023Review
- An Insight into miR-1290: An Oncogenic miRNA with Diagnostic Potential.International journal of molecular sciences · 2022Review
- Recent Insight on Regulations of FBXW7 and Its Role in Immunotherapy.Frontiers in oncology · 2022Review
- Implications of FBXW7 in Neurodevelopment and Neurodegeneration: Molecular Mechanisms and Therapeutic Potential.Frontiers in cellular neuroscience · 2021Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Dysregulated circular RNAs (circRNAs) have been confirmed to partake in the modulation of the glioma progression. Here, we intended to explore the role of circBRAF in glioma and the possible action mechanism. The expression levels of circBRAF, microRNA (miR)-1290 and F-box and WD repeat domain containing 7 (FBXW7) were analyzed by quantitative reverse transcription polymerase chain reaction (qRT-PCR) or western blot. Cell viability was assessed by 3-(4, 5)-dimethylthiazole-2-y1)-2, 5-biphenyl tetrazolium bromide (MTT) assay. Cell cycle distribution was determined by flow cytometry. Cell migration and invasion were evaluated through Trans-well assay. Related protein levels were detected by western blot. Targeted relation among circBRAF, miR-1290 and FBXW7 was validated by dual-luciferase reporter, RNA immunoprecipitation (RIP) and pull-down assays. Xenograft model was constructed to explore the function of circBRAF in vivo. Expression of circBRAF and FBXW7 was decreased in glioma tissues and cells. Upregulation of circBRAF inhibited glioma cell proliferation and metastasis in vitro. MiR-1290 was upregulated in glioma, which was sponged by circBRAF. Besides, circBRAF elevated FBXW7 expression by targeting miR-1290. Introduction of miR-1290 or FBXW7 knockdown could counteract the inhibitory effects of circBRAF upregulation on the malignant phenotypes of glioma cells. Overexpression of circBRAF repressed the tumor growth in vivo. Upregulation of circBRAF suppressed glioma evolvement in vitro and in vivo by regulating miR-1290/FBXW7 axis, broadening the cognition of glioma progression.
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