ArticleThoracic cancer2024
CircSEC24A induces KLF8 expression to promote the malignant progression of non-small cell lung cancer by regulating miR-1253.
Article in Thoracic cancer, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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Who cites it
4 citing papers in PubMed.
- Circular RNA hsa_circ_0003472 Promotes Pancreatic Ductal Adenocarcinoma Progression and Gemcitabine Resistance Via the mir-1253/ERCC1 Axis.Biological procedures online · 2026Article
- The long noncoding RNA AC093895.1 promotes ovarian cancer formation and metastasis through a positive feedback network dependent on the transcription factor SOX4.Cell death & disease · 2026Article
- Review
- CircSEC24A induces KLF8 expression to promote the malignant progression of non-small cell lung cancer by regulating miR-1253.Thoracic cancer · 2024Article
Corrections and comments
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Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectivesThis study aimed to analyze the role of circSEC24A in non-small cell lung cancer (NSCLC) and its underlying mechanism.
methodsRNA levels of circSEC24A, microRNA-1253 (miR-1253), and KLF transcription factor 8 (KLF8) were detected by quantitative real-time polymerase chain reaction. Protein expression was analyzed by western blot or immunohistochemistry assay. Cell proliferation and apoptosis were investigated by colony formation assay, 5-ethynyl-2'-deoxyuridine assay, and flow cytometry analysis. Glycolysis was evaluated by commercial kits. Dual-luciferase reporter assay and RNA immunoprecipitation assay were conducted to identify the associations among circSEC24A, miR-1253, and KLF8. Xenograft mouse model assay was used to evaluate the effect of circSEC24A on tumor tumorigenesis.
resultsCircSEC24A and KLF8 were upregulated, while miR-1253 was downregulated in NSCLC. CircSEC24A knockdown inhibited proliferation and glycolysis but induced the apoptosis of NSCLC cells. CircSEC24A acted as a miR-1253 sponge and regulated NSCLC cell malignancy by targeting miR-1253. KLF8 was identified as a target of miR-1253, and its overexpression attenuated miR-1253-induced effects in NSCLC cells. Besides, circSEC24A upregulated KLF8 by sponging miR-1253. Further, circSEC24A knockdown suppressed NSCLC cell tumorigenesis in vivo.
conclusionsCircSEC24A silencing inhibited NSCLC cell malignancy through the miR-1253/KLF8 pathway, providing a potential therapeutic target for NSCLC.
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