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IncRNA MIAT Accelerates Keloid Formation by miR-411-5p/JAG1 Axis

Yingyan Yu1, Yujie Dong2, Benyuan Deng3

  • 1Department of Dermatology, University of Electronic Science and Technology of China Hospital, Chengdu 611731, Sichuan, China.

Critical Reviews in Eukaryotic Gene Expression
|February 3, 2023
PubMed

Insights

The long non-coding RNA MIAT promotes keloid formation by sponging miR-411-5p, which targets JAG1. This mechanism highlights MIAT

Area of Science:

  • Molecular Biology
  • Dermatology
  • RNA Biology

Background:

  • Long non-coding RNA (lncRNA) myocardial infarction-associated transcript (MIAT) influences cellular functions.
  • Keloids are abnormal scars resulting from excessive fibroblast proliferation and extracellular matrix deposition.
  • The role of MIAT in keloid pathogenesis remains largely unexplored.

Purpose of the Study:

  • To investigate the mechanism by which MIAT affects keloid progression.
  • To elucidate the interaction between MIAT, JAG1, and miR-411-5p in keloid fibroblasts (KEL FIBs).

Main Methods:

  • Quantitative reverse transcription polymerase chain reaction (qRT-PCR) and Western blot to assess gene and protein expression.
  • Cell proliferation, migration, and invasion assays (CCK-8, wound healing, Transwell).
  • Luciferase reporter and RNA immunoprecipitation (RIP) assays to confirm molecular interactions.

Main Results:

  • MIAT and JAG1 were upregulated, while miR-411-5p was downregulated in keloid tissues and KEL FIBs.
  • Knockdown of MIAT or JAG1 inhibited KEL FIB proliferation, migration, and invasion.
  • Suppression of miR-411-5p enhanced these cellular functions.
  • MIAT directly sponges miR-411-5p, and miR-411-5p targets JAG1.

Conclusions:

  • MIAT accelerates keloid formation by modulating the miR-411-5p/JAG1 axis.
  • MIAT acts as a competing endogenous RNA (ceRNA) for miR-411-5p, upregulating JAG1.
  • Targeting the MIAT/miR-411-5p/JAG1 pathway may offer a therapeutic strategy for keloids.

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