SNHG16 promotes the progression of osteoarthritis through activating microRNA-93-5p/CCND1 axis

W Cheng1, C-Y Hao, S Zhao

  • 1Department of Orthopedics, The First Affiliated Hospital of Jinzhou Medical University, Jinzhou, China. liudan5900@163.com.

Abstract

Insights

Small nucleolar RNA host gene 16 (SNHG16) promotes osteoarthritis (OA) by upregulating Cyclin D1 (CCND1) via downregulating microRNA-93-5p. This highlights SNHG16 as a potential therapeutic target for OA treatment.

Area of Science:

  • Molecular Biology
  • Biochemistry
  • Orthopedics

Background:

  • Osteoarthritis (OA) is a degenerative joint disease with limited therapeutic options.
  • Understanding the molecular mechanisms driving OA progression is crucial for developing effective treatments.

Purpose of the Study:

  • To investigate the role of small nucleolar RNA host gene 16 (SNHG16) in OA pathogenesis.
  • To determine if SNHG16 promotes OA by regulating the microRNA-93-5p/Cyclin D1 (CCND1) axis.
  • To identify SNHG16 as a potential therapeutic target for OA.

Main Methods:

  • Quantitative Real-Time Polymerase Chain Reaction (qRT-PCR) to measure gene expression in OA and control cartilage tissues.
  • Cell Counting Kit-8 (CCK-8), colony formation assay, and flow cytometry to assess chondrocyte proliferation and cell cycle.
  • Dual-Luciferase reporter gene assay to confirm molecular interactions.
  • Rescue experiments to validate the regulatory pathway.

Main Results:

  • SNHG16 and CCND1 were upregulated, while microRNA-93-5p was downregulated in OA cartilage.
  • SNHG16 knockdown inhibited chondrocyte viability, proliferation, and cell cycle progression.
  • SNHG16 directly targets microRNA-93-5p, and microRNA-93-5p targets CCND1.
  • SNHG16 promotes OA development by upregulating CCND1 through the suppression of microRNA-93-5p.

Conclusions:

  • SNHG16 plays a critical role in promoting osteoarthritis development.
  • The SNHG16/microRNA-93-5p/CCND1 axis is a key pathway in OA pathogenesis.
  • Targeting SNHG16 offers a promising therapeutic strategy for osteoarthritis.

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