ArticleCancer cell international2020
Long noncoding RNA SNHG17 induced by YY1 facilitates the glioma progression through targeting miR-506-3p/CTNNB1 axis to activate Wnt/β-catenin signaling pathway.
Article in Cancer cell international, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 54 citations in OpenAlex.
- Exploration of the Potential Mechanisms of Yinqiao Powder in Treating Atopic Dermatitis: Integrating Network Pharmacology, Single-Cell, and Bulk RNA Sequencing.Journal of asthma and allergy · 2026Trial
- Machine learning on transcription factor expression profiles for precision breast cancer therapy.Cancer cell international · 2025Article
- Yin Yang 1: Function, Mechanisms, and Glia.Neurochemical research · 2025Review
- Association ofGynecology and pelvic medicine · 2025Article
- Therapeutic potential of microRNA-506 in cancer treatment: mechanisms and therapeutic implications.Frontiers in oncology · 2025Review
- Review
- YY1-induced lncRNA00511 promotes melanoma progression via the miR-150-5p/ADAM19 axis.American journal of cancer research · 2024Article
- Article
- Targeting Transcription Factor YY1 for Cancer Treatment: Current Strategies and Future Directions.Cancers · 2023Review
- Transcription factor YY1 mediates self-renewal of glioblastoma stem cells through regulation of the SENP1/METTL3/MYC axis.Cancer gene therapy · 2023Article
- Interplay between lncRNA/miRNA and Wnt/ß-catenin signaling in brain cancer tumorigenesis.EXCLI journal · 2023Review
- Crosstalk between YY1 and lncRNAs in cancer: A review.Medicine · 2022Review
- Circular RNA circPTPRF promotes the progression of GBM via sponging miR-1208 to up-regulate YY1.Cancer cell international · 2022Article
- CircPTK2 accelerates tumorigenesis of colorectal cancer by upregulating AKT2 expression via miR-506-3p.The Kaohsiung journal of medical sciences · 2022Article
- m6A methyltransferase METTL3-induced lncRNA SNHG17 promotes lung adenocarcinoma gefitinib resistance by epigenetically repressing LATS2 expression.Cell death & disease · 2022Article
- YY1 accelerates oral squamous cell carcinoma progression through long non-coding RNA Kcnq1ot1/microRNA-506-3p/SYPL1 axis.Journal of ovarian research · 2022Article
- LncRNA LINC01410 Induced by MYC Accelerates Glioma Progression via Sponging miR-506-3p and Modulating NOTCH2 Expression to Motivate Notch Signaling Pathway.Cellular and molecular neurobiology · 2022Article
- Long noncoding RNA SNHG17: a novel molecule in human cancers.Cancer cell international · 2022Review
- Enabling factor for cancer hallmark acquisition: Small nucleolar RNA host gene 17.Frontiers in oncology · 2022Review
- SNHG17, as an EMT-related lncRNA, promotes the expression of c-Myc by binding to c-Jun in esophageal squamous cell carcinoma.Cancer science · 2022Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundGlioma is one of the most widely diagnosed malignancies worldwide. It has been reported that long noncoding RNAs (lncRNAs) are participators in the tumorgenesis of cancers. Nevertheless, the role and function of lncRNA SNHG17 among glioma is unclear.
methodsRT-qPCR revealed SNHG17, YY1, miR-506-3p, CTNNB1 expression among glioma cells. CCK-8, colony formation, EdU, flow cytometry, TUNEL and western blot assays revealed the function of SNHG17 in glioma. RIP uncovered SNHG17, miR-506-3p and CTNNB1 enrichment in RISC complex. Luciferase reporter assays and RNA pull down revealed interaction of miR-506-3p with SNHG17 and CTNNB1.
resultsSNHG17 expression was up-regulated in glioma tissues and cells. SNHG17 silence attenuated cell proliferation and promoted apoptosis and repressed tumor growth. Moreover, SNHG17 was up-regulated by transcription factor YY1. Mechanistically, SNHG17 activated Wnt/β-catenin signaling pathway in glioma. CTNNB1 was referred to as the mRNA of β-catenin, we validated that SNHG17 bound to miR-506-3p to induce CTNNB1 and activate Wnt/β-catenin signaling pathway. Rescue experiments indicated that CTNNB1 overexpression abolished the inhibitory effects of SNHG7 inhibition on glioma progression.
conclusionsThe findings that YY1-induced SNHG17 facilitated the glioma progression through targeting miR-506-3p/CTNNB1 axis to activate Wnt/β-catenin signaling pathway offered a brand-new prospects to molecular-targeted treatment for glioma.
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