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RNA Pull-down Procedure to Identify RNA Targets of a Long Non-coding RNA
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Long non-coding RNA SNHG7 promotes the fracture repair through negative modulation of miR-9

Zhiqing Chen1,2,3,4, Zhi Liu1,2,3,4, Lin Shen5

  • 1Department of Osteology, Tianjin Third Central Hospital Tianjin 300170, China.

American Journal of Translational Research
|March 23, 2019
PubMed

Insights

Long non-coding small nucleolar RNA host gene 7 (SNHG7) promotes bone repair in femoral neck fractures. Lower SNHG7 levels inhibit osteoblast activity and hinder fracture healing, suggesting SNHG7 as a therapeutic target.

Area of Science:

  • Orthopedics
  • Molecular Biology
  • Biochemistry

Background:

  • Fracture is a prevalent orthopedic condition.
  • Long non-coding RNA host gene 7 (SNHG7) is implicated in cancer progression.
  • The function of SNHG7 in skeletal fracture healing is not well understood.

Purpose of the Study:

  • To investigate the role of SNHG7 in femoral neck fracture healing.
  • To elucidate the molecular mechanisms underlying SNHG7's function in osteoblasts.

Main Methods:

  • Analysis of SNHG7 expression in fracture tissues.
  • In vitro studies involving SNHG7 knockdown in osteoblast cells.
  • Bioinformatic analysis to identify miRNA targets and signaling pathways.

Main Results:

  • SNHG7 expression was decreased in femoral neck fracture tissues.
  • SNHG7 knockdown impaired osteoblast proliferation, migration, and activity, while inducing apoptosis.
  • SNHG7 was identified as a molecular sponge for miR-9, which targets TGFBR2.
  • SNHG7 knockdown suppressed the TGF-β signaling pathway.

Conclusions:

  • SNHG7 plays a crucial role in promoting bone repair in femoral neck fractures.
  • SNHG7 facilitates osteoblast function and survival through the miR-9/TGFBR2/TGF-β pathway.
  • SNHG7 represents a potential therapeutic target for enhancing bone formation and fracture healing.
Keywords:
Femoral neck fractureSNHG7TGF-β signaling pathwaymiR-9osteoblast cells

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