ArticleBioengineered2022
Long non-coding RNA nuclear-enriched abundant transcript 1 (LncRNA NEAT1) upregulates Cyclin T2 (CCNT2) in laryngeal papilloma through sponging miR-577/miR-1224-5p and blocking cell apoptosis.
Article in Bioengineered, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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7 citing papers in PubMed, 13 citations in OpenAlex.
- Emerging roles of non-coding RNAs in modulating the PI3K/Akt pathway in cancer.Non-coding RNA research · 2025Review
- Identification of the microglia-associated signature in experimental autoimmune encephalomyelitis.Frontiers in immunology · 2025Article
- Circ_0007386 Promotes the Progression of Hepatocellular Carcinoma Through the miR-507/ CCNT2 Axis.Journal of hepatocellular carcinoma · 2024Article
- Preclinical Models of Laryngeal Papillomavirus Infection: A Scoping Review.The Laryngoscope · 2023Article
- Article
- LncRNA growth arrest specific transcript 5 inhibits the growth of pituitary neuroendocrine tumors via miR-27a-5p/cylindromatosis axis.Bioengineered · 2022Article
- Long intergenic non-protein coding RNA 847 promotes laryngeal squamous cell carcinoma progression through the microRNA-181a-5p/zinc finger E-box binding homeobox 2 axis.Bioengineered · 2022Article
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2 authors at 1 institution in 1 country.
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Abstract
Long non-coding RNA nuclear-enriched abundant transcript 1 (Lnc-NEAT1) is a crucial mediator in cancer progression, which is associated with poor prognosis of patients with laryngeal papilloma (LP). Herein, we aimed to determine how Lnc-NEAT1 promotes LP development. q-PCR, MTT, EDU and Western blotting were performed to determine that Lnc-NEAT1 facilitates LP cell proliferation and hinders cell apoptosis. LncBase database, q-PCR, GEPIA online database, Dual luciferase reporter and RIP assays were utilized to confirm that Lnc-NEAT1 sponged miR-577/miR-1224-5p and negatively mediated CCNT2. Western blotting, MTT and EDU were used to confirm that Lnc-NEAT1 promoted LP cell proliferation and inhibited cell apoptosis through CCNT2. Lnc-NEAT1 was highly expressed in LP, and enhanced LP cell proliferation, and it was inhibited by Lnc-NEAT1 depleting. Concerning the underlying mechanism, it was found that Lnc-NEAT1 could functionally sponge microRNA-577 (miR-577) and microRNA-1224-5p (miR-1224-5p) and up-regulate Cyclin T2 (CCNT2) in LP cells. Notably, CCNT2 knockdown blocked Lnc-NEAT1-induced LP cell proliferation, and rescued cell apoptosis, which was specifically indicated by restoration of Bax, Cleaved caspase 3 and Cleaved caspase 9. Lnc-NEAT1 played a carcinogenic role in LP through mediating miR-577 or miR-1224-5p/CCNT2 axis, which may provide promising insights for the treatment of LP.
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