ArticleThoracic cancer2021
Circ_0016760 accelerates non-small-cell lung cancer progression through miR-646/AKT3 signaling in vivo and in vitro.
Article in Thoracic cancer, 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, 15 citations in OpenAlex.
- Bio-engineered microRNA-7 effectively interferes with the Akt3/p53 axis to suppress human non-small cell lung cancer.Cancer cell international · 2025Article
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- [Overexpression of lncRNA FEZF1-AS1 promotes progression of non-small cell lung cancerNan fang yi ke da xue xue bao = Journal of Southern Medical University · 2024Article
- CircWHSC1 (CircNSD2): A Novel Circular RNA in Multiple Cancers.Clinical Medicine Insights. Oncology · 2024Review
- Circular RNA in Non-small Cell Lung Carcinoma: Identification of Targets and New Treatment Modalities.Cancer genomics & proteomics · 2023Review
- Review
- Macrophages depletion alleviates lung injury by modulating AKT3/GXP4 following ventilator associated pneumonia.Frontiers in immunology · 2023Article
- Circular RNAs modulate Hippo-YAP signaling: functional mechanisms in cancer.Theranostics · 2022Review
- Circ_0016760 accelerates non-small-cell lung cancer progression through miR-646/AKT3 signaling in vivo and in vitro.Thoracic cancer · 2021Article
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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
backgroundCurrently, the prognosis of non-small-cell lung cancer (NSCLC) patients remains dismal due to recurrence and metastasis. The purpose of our study was to explore the role of circular RNA_0016760 (circ_0016760) in NSCLC progression and its associated mechanism.
methodsQuantitative real-time polymerase chain reaction (qRT-PCR) was implemented to measure the expression of circ_0016760, microRNA-646 (miR-646) and AK strain thymoma serine/threonine kinase 3 (AKT3). The protein level of AKT3 was examined by Western blot assay. Cell Counting Kit 8 assay, transwell assays, and flow cytometry were conducted to analyze cell proliferation, metastasis, and apoptosis. Dual-luciferase reporter assay was used to confirm the interactions that were predicted by bioinformatics software (Circular RNA Interactome and TargetScan). A xenograft tumor model was built to investigate the role of circ_0016760 in vivo.
resultsCirc_0016760 and AKT3 were highly expressed in NSCLC tissue specimens and cell lines. Circ_0016760 interference suppressed cell proliferation, migration, and invasion and promoted the apoptosis of NSCLC cells. Circ_0016760 interacted with miR-646 and negatively regulated its expression. MiR-646 silencing partly counteracted circ_0016760 knockdown-mediated influences in NSCLC cells. MiR-646 bound to the AKT3 3' untranslated region in NSCLC cells, and miR-646 overexpression-induced effects in NSCLC cells were partly overturned by the addition of AKT3 overexpression plasmid. Circ_0016760 silencing reduced the expression of AKT3 through enhancing miR-646 expression. Circ_0016760 knockdown suppressed NSCLC tumor growth in vivo.
conclusionCirc_0016760 played an oncogenic role to promote the proliferation, migration, and invasion and restrained the apoptosis of NSCLC cells via miR-646/AKT3 signaling.
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