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The circRHOBTB3/EIF4A3/NF-κB Axis Promotes Progression of Atopic Dermatitis

Haodong Chen1, Jinqi Hao1, Yang Zhang2

  • 1Baotou Medical College of Inner Mongolia University of Science and Technology, Baotou 014040, China.

Critical Reviews in Eukaryotic Gene Expression
|October 24, 2025
PubMed

Insights

Circular RNAs (circRNAs) play a key role in atopic dermatitis (AD). This study found that circRHOBTB3 promotes AD by activating the NF-κB signaling pathway, suggesting circRHOBTB3 as a potential therapeutic target for AD.

Area of Science:

  • Dermatology
  • Molecular Biology
  • Immunology

Background:

  • Circular RNAs (circRNAs) are implicated in the pathogenesis of atopic dermatitis (AD).
  • The specific role of circRHOBTB3 in AD progression remains unclear.
  • Understanding the molecular mechanisms underlying circRHOBTB3's function in AD is crucial for developing targeted therapies.

Purpose of the Study:

  • To investigate the role and mechanism of circRHOBTB3 in the development of atopic dermatitis (AD).
  • To elucidate the interaction between circRHOBTB3, EIF4A3, and NF-κB signaling in AD pathogenesis.
  • To evaluate circRHOBTB3 as a potential therapeutic target for AD.

Main Methods:

  • Established an in vitro AD model using human keratinocytes (HaCaT) stimulated with IL-4.
  • Quantified gene and protein expression via RT-qPCR and Western blot.
  • Assessed cytokine release using ELISA, cellular localization with FISH, and molecular interactions using RIP, RNA pull-down, luciferase, and ChIP assays.
  • Evaluated cellular functions including proliferation and migration using CCK-8, colony formation, wound healing, and Transwell assays.

Main Results:

  • circRHOBTB3 expression was upregulated in response to TNF-α/IFN-γ treatment in HaCaT cells.
  • Knockdown of circRHOBTB3 inhibited inflammatory responses and keratinocyte proliferation.
  • circRHOBTB3 interacts with EIF4A3 to activate NF-κB signaling, which in turn promotes circRHOBTB3 transcription, forming a positive feedback loop.
  • Overexpression of NF-κB exacerbated inflammation and proliferation in HaCaT cells.

Conclusions:

  • The circRHOBTB3/EIF4A3/NF-κB axis forms a positive feedback loop that drives inflammation and proliferation in atopic dermatitis.
  • Inhibition of circRHOBTB3 effectively suppresses keratinocyte inflammatory responses and proliferation.
  • Targeting circRHOBTB3 presents a promising therapeutic strategy for managing atopic dermatitis.

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