ArticleBosnian journal of basic medical sciences2022
LncRNA ADAMTS9-AS1 knockdown suppresses cell proliferation and migration in glioma through downregulating Wnt/β-catenin signaling pathway.
Article in Bosnian journal of basic medical sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 9 citations in OpenAlex.
- Exploring the Role of Long Non-Coding RNAs in Mediating Cisplatin Resistance in Glioma/Glioblastoma Cells.International journal of molecular sciences · 2026Review
- Transitioning from molecular methods to therapeutic methods: An in‑depth analysis of glioblastoma (Review).Oncology reports · 2025Review
- Emerging roles of non-coding RNAs in modulating the PI3K/Akt pathway in cancer.Non-coding RNA research · 2025Review
- The Dual Role of ADAMTS9-AS1 in Various Human Cancers: Molecular Pathogenesis and Clinical Implications.Anti-cancer agents in medicinal chemistry · 2025Review
- The pathogenesis mechanism and potential clinical value of lncRNA in gliomas.Discover oncology · 2024Review
- Function of Long Noncoding RNAs in Glioma Progression and Treatment Based on the Wnt/β-Catenin and PI3K/AKT Signaling Pathways.Cellular and molecular neurobiology · 2023Review
- ADAMTS9-AS1 Long Non‑coding RNA Sponges miR‑128 and miR-150 to Regulate Ras/MAPK Signaling Pathway in Glioma.Cellular and molecular neurobiology · 2023Article
- Interplay between lncRNA/miRNA and Wnt/ß-catenin signaling in brain cancer tumorigenesis.EXCLI journal · 2023Review
- Mechanisms of long non-coding RNAs in biological phenotypes and ferroptosis of glioma.Frontiers in oncology · 2022Review
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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
The long non-coding RNA antisense 1 ADAMTS9-AS1 has been reported to serve as an oncogene or tumor suppressor in several tumors, including colorectal cancer and hepatocellular carcinoma. Nevertheless, the clinical significance and biological behaviors of ADAMTS9-AS1 in glioma still remain unclear. Therefore, the goal of this study was to evaluate the functional roles and potential mechanisms of ADAMTS9-AS1 in glioma cells. Using quantitative real-time PCR analysis, we found that ADAMTS9-AS1 was upregulated in glioma tissues and cells in comparison to corresponding controls. ADAMTS9-AS1 expression level was correlated to tumor size (p=0.005) and WHO grade (p=0.002). Kaplan-Meier analysis and Cox multivariate analysis showed that ADAMTS9-AS1 could serve as an independent prognostic factor affecting the overall survival of glioma patients. Functionally, depletion of ADAMTS9-AS1 significantly suppressed the proliferation, migration and invasion in glioma cell lines (U251 and U87), as shown via CCK-8 assay, Edu corporation assay, wound healing assay and transwell assay. Furthermore, we demonstrated that knockdown of ADAMTS9-AS1 suppressed Wnt1, β-catenin, c-myc and PCNA, while upregulating E-cadherin expression. In conclusion, our data revealed that ADAMTS9-AS1 confers oncogenic function in the progression of glioma, thus targeting ADAMTS9-AS1 might be a promising therapeutic strategy for this disease.
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