ArticleEuropean journal of medical research2025
circZNF707 promoted glycolysis and tumor progression through miR-668-3p-PFKM axis in NSCLC.
Article in European journal of medical research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
5 citing papers in PubMed.
- Circular RNAs in NSCLC: Their Role in Tumorigenesis, Tumor Microenvironment Reshaping, and Response to Therapies.Cancers · 2026Review
- Circ-PRKCI attenuates acute lung injury secondary to sepsis by targeting the miR-106b-5p/GAB1 axis.European journal of medical research · 2026Article
- Metabolic reprogramming and lung cancer focused on roles, mechanism, and clinical prospects of circRNAs: a narrative review.Frontiers in oncology · 2026Review
- MiR-668-3p in M2 macrophage-derived exosomes activates autophagy through the ETS1/EGFR axis and promotes cisplatin resistance in gastric cancer.Cancer cell international · 2025Article
- Review
Corrections and comments
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Authors and funding
9 authors.
Funding
Abstract
backgroundCircular RNA (circRNA) plays an important regulatory role in the development of human malignancies, but the potential mechanisms of circRNA in non-small cell lung cancer (NSCLC) remain largely unknown.
methodsMicroarray analysis was used to test for circRNAs differing in expression between NSCLC tumors and healthy adjacent tissues. Using qRT-PCR, the expression of circZNF707 was determined. Through a number of loss-of-function and gain-of-function investigations, the biological behavior of NSCLC cells was evaluated. Finally, tests using Western blotting, RIP, qRT-PCR, and luciferase reporter gene detection and rescue assays revealed the potential mechanism of circZNF707.
resultsIncreased expression of circZNF707 was found in NSCLC tissues. Functionally, circZNF707 enhances proliferation, migration, invasion, and glycolysis of NSCLC cells. Mechanistically, circZNF707 can upregulate PFKM by acting as a sponge for miR-668-3p, thus contributing to the progression of NSCLC.
conclusionsThrough the circZNF707/miR-668-3p/PFKM axis, upregulation of circZNF707 promotes tumor development. CircZNF707 may provide new insights into the treatment and diagnosis of NSCLC.
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