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The stimulative function of long noncoding RNA CDKN2B-AS1 in osteosarcoma by targeting the microRNA-122/CCNG1 axis
Abulaiti Abula1, Guliayixiamu Saimaiti2, Xayimardan Maimaiti1
1Department of Microrepair and Reconstruction, the First Affiliated Hospital of Xinjiang Medical University, Xinjiang, P.R China.
Abstract:
Osteosarcoma (OS), a prevalent aggressive malignancy in the bone, has limited therapeutic targets and diagnostic biomarkers. In the current investigation, RT-qPCR showed that CDKN2B-AS1 was enhanced in OS samples and cells. This research was set to examine the modulation of CDKN2B-AS1 in OS. The expression of CDKN2B-AS1 and downstream molecules was analyzed by RT-qPCR method. CCK8, EdU staining along with Transwell assays were applied to evaluate cell proliferation and invasion. Those in vitro investigations specified that silencing of CDKN2B-AS1 with shRNAs obviously impeded the proliferation and invasion of MG63 cells. To authenticate the relationships between CDKN2B-AS1 and microRNA-122-5p (miR-122-5p) or cyclin G1 (CCNG1) and miR-122-5p, we next employed luciferase reporter assay. We displayed that CDKN2B-AS1 repressed miR-122-5p to restore CCNG1 expression. All in all, our findings substantiated the indispensable function of CDKN2B-AS1 in OS progression and the possible molecular mechanism.
Insights
CDKN2B-AS1 is elevated in osteosarcoma (OS) and drives cancer progression by inhibiting miR-122-5p, which restores cyclin G1 expression. Silencing CDKN2B-AS1 hinders OS cell proliferation and invasion.
Area of Science:
- Oncology
- Molecular Biology
- Biochemistry
Background:
- Osteosarcoma (OS) is an aggressive bone cancer with limited therapeutic options.
- Identifying novel molecular targets and biomarkers is crucial for OS treatment.
- The role of CDKN2B-AS1 in OS pathogenesis requires further elucidation.
Purpose of the Study:
- To investigate the role and molecular mechanism of CDKN2B-AS1 in osteosarcoma.
- To determine the impact of CDKN2B-AS1 modulation on OS cell behavior.
- To explore the regulatory relationship between CDKN2B-AS1, miR-122-5p, and CCNG1.
Main Methods:
- Quantitative real-time PCR (RT-qPCR) to assess gene expression.
- Cell Counting Kit-8 (CCK8), EdU staining, and Transwell assays for proliferation and invasion.
- Luciferase reporter assay to validate molecular interactions.
Main Results:
- CDKN2B-AS1 expression was significantly upregulated in OS tissues and cells.
- Silencing CDKN2B-AS1 using shRNAs inhibited MG63 cell proliferation and invasion.
- CDKN2B-AS1 was found to repress miR-122-5p, leading to the restoration of CCNG1 expression.
Conclusions:
- CDKN2B-AS1 plays a critical role in promoting osteosarcoma progression.
- The molecular mechanism involves the repression of miR-122-5p and subsequent upregulation of CCNG1.
- CDKN2B-AS1 represents a potential therapeutic target for osteosarcoma.
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