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LncRNA PLCD3-OT1 Functions as a CeRNA to Prevent Age-Related Cataract by Sponging miR-224-5p and Regulating PLCD3

Jing Xiang1,2, Qin Chen3, Lihua Kang1

  • 1Eye Institute, Affiliated Hospital of Nantong University, Nantong, Jiangsu Province, China.

Abstract

Insights

Long noncoding RNA PLCD3-OT1 is decreased in age-related cataract (ARC). Its overexpression promotes cell viability and proliferation, suggesting PLCD3-OT1 and PLCD3 as potential therapeutic targets for ARC.

Area of Science:

  • Ophthalmology
  • Molecular Biology
  • Genetics

Background:

  • Long noncoding RNAs (lncRNAs) play critical roles in cellular functions and disease progression.
  • Age-related cataract (ARC) is a leading cause of vision impairment globally.
  • Understanding the molecular mechanisms underlying ARC is crucial for developing effective treatments.

Purpose of the Study:

  • To perform global lncRNA profiling in age-related cataract (ARC).
  • To investigate the role of lncRNA 1-phosphatidylinositol-4,5-bisphosphate phosphodiesterase delta 3-sence RNA 1 (PLCD3-OT1) in ARC progression.

Main Methods:

  • High-throughput RNA-sequencing for lncRNA expression profiling in lens capsule samples.
  • Real-time PCR to validate lncRNA and mRNA expression in clinical samples and cell models.
  • Cellular assays (CCK-8, EdU, TUNEL, PI staining) to assess cell viability, proliferation, and apoptosis.

Main Results:

  • lncRNA PLCD3-OT1 and its target gene PLCD3 expression were significantly decreased in ARC.
  • Overexpression of PLCD3-OT1 enhanced cell viability, proliferation, and inhibited apoptosis under oxidative stress.
  • PLCD3-OT1 positively regulates PLCD3 expression, potentially acting as a competing endogenous RNA (ceRNA) for miR-224-5p.

Conclusions:

  • PLCD3-OT1 plays a protective role in age-related cataract progression.
  • PLCD3-OT1 and PLCD3 represent potential therapeutic targets for ARC diagnosis and treatment.

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