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.

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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