ArticleBioengineered2022
Circ_0020123 enhances the cisplatin resistance in non-small cell lung cancer cells partly by sponging miR-140-3p to regulate homeobox B5 (HOXB5).
Article in Bioengineered, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 12 citations in OpenAlex.
- NK-cell-derived exosomes exert antitumor potency via miR-140/XYLT1/HSPG2 axis.Cellular & molecular biology letters · 2026Article
- HOXB5 in precision oncology: regulatory networks, functional duality, and clinical prospects.Journal of translational medicine · 2026Review
- *Mechanisms of circular RNA in drug resistance of lung cancer: therapeutic targets, biomarkers, and future research directions.Discover oncology · 2025Review
- Emerging roles of CircRNA-miRNA networks in cancer development and therapeutic response.Non-coding RNA research · 2025Review
- Extracellular Vesicles in Lung Cancer: Implementation in Diagnosis and Therapeutic Perspectives.Cancers · 2024Review
- Article
- CARD9 contributes to ovarian cancer cell proliferation, cycle arrest, and cisplatin sensitivity.BMC molecular and cell biology · 2022Article
- The emerging role of circular RNAs in drug resistance of non-small cell lung cancer.Frontiers in oncology · 2022Review
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
Cisplatin (DDP) therapy is widely used for the treatment of non-small cell lung cancer (NSCLC), but the curative effect is limited by chemoresistance. This study was designed to explore circ_0020123 function in DDP resistance of NSCLCDDP. Expression detection for circ_0020123, microRNA-140-3p (miR-140-3p) and homeobox B5 (HOXB5) was performed by real-time polymerase chain reaction (qRT-PCR). Half inhibitory concentration (IC50) of DDP and cell proliferation was detected by Cell Counting Kit-8 (CCK-8) assay. Colony formation ability was assessed using colony formation assay. Cell migration and invasion were evaluated via transwell assay. Cell apoptosis was examined by flow cytometry. Protein analysis was conducted by Western blot. Dual-luciferase reporter assay was used to affirm target interaction. Circ_0020123 expression was upregulated in DDP-resistant NSCLC cells. DDP resistance was reduced by downregulation of circ_0020123 in NSCLC cells. Circ_0020123 was identified as a miR-140-3p sponge. The effect of si-circ_0020123 on DDP resistance was partly associated with miR-140-3p upregulation. HOXB5 was a downstream target for miR-140-3p. Overexpression of HOXB5 mitigated miR-140-3p-induced inhibition of DDP resistance in NSCLC cells. Circ_0020123 upregulated the level of HOXB5 partly via sponging miR-140-3p. Also, circ_0020123 promoted tumor growth in NSCLC/DDP xenografts by regulating miR-140-3p and HOXB5 levels at least in part. These results revealed that circ_0020123 promoted DDP resistance in NSCLC cells partly by targeting miR-140-3p/HOXB5 axis, indicating that circ_0020123 might be used as a molecular target in DDP treatment for NSCLC.
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