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MiR-103-3p targets the m6 A methyltransferase METTL14 to inhibit osteoblastic bone formation

Zhongyang Sun1,2, Han Wang3, Yuxiang Wang1

  • 1Department of Orthopedics, Affiliated Jinling Hospital, Medical School of Nanjing University, Nanjing, China.

Aging Cell
|January 13, 2021
PubMed

Insights

MicroRNA-103-3p impairs bone formation by inhibiting osteoblast activity. Targeting this microRNA and its interaction with METTL14 and m6A methylation may offer new osteoporosis treatments.

Area of Science:

  • Molecular Biology
  • Cell Biology
  • Bone Biology

Background:

  • Osteoporosis is linked to impaired osteoblast function.
  • MicroRNA (miRNA) dysregulation can disrupt osteoblast activity, but mechanisms are unclear.

Purpose of the Study:

  • Investigate the role of miR-103-3p in osteoblast activity and bone formation.
  • Elucidate the molecular mechanisms involving miR-103-3p, METTL14, and N6-methyladenosine (m6A) methylation in osteoporosis.

Main Methods:

  • Correlation analysis in human bone specimens and ovariectomized (OVX) mouse models.
  • In vivo and in vitro experiments to assess miR-103-3p targeting of Mettl14.
  • Analysis of METTL14-dependent m6A methylation's effect on miR-103-3p processing and osteoblast activity.

Main Results:

  • miR-103-3p negatively correlated with bone formation and osteoblast activity.
  • miR-103-3p directly targets Mettl14, inhibiting osteoblast function.
  • METTL14-dependent m6A methylation promotes osteoblast activity by inhibiting miR-103-3p processing.
  • Inhibition of miR-103-3p in OVX mice improved bone formation.

Conclusions:

  • The miR-103-3p/METTL14/m6A signaling axis is crucial for osteoblast activity.
  • This axis represents a potential therapeutic target for osteoporosis treatment.
Keywords:
METTL14N6-methyladenosinemiR-103-3posteoblast activityosteoporosis

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