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Updated: Oct 6, 2025

Screening for Functional Non-coding Genetic Variants Using Electrophoretic Mobility Shift Assay EMSA and DNA-affinity Precipitation Assay DAPA
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LncRNA Dlx6os1 Accelerates Diabetic Nephropathy Progression by Epigenetically Repressing SOX6 via Recruiting EZH2

Yan-Xia Chen1, Shu-Ying Zhu1, Chong Huang1

  • 1Department of Nephrology, The Second Affiliated Hospital of Nanchang University, Nanchang, China.

Kidney & Blood Pressure Research
|January 17, 2022
PubMed
Abstract

Insights

Diabetic nephropathy (DN) progresses due to lncRNA Dlx6os1. This long non-coding RNA accelerates DN by epigenetically silencing SOX6 through EZH2 recruitment, highlighting a potential therapeutic target.

Area of Science:

  • Molecular Biology
  • Nephrology
  • Epigenetics

Background:

  • Diabetic nephropathy (DN) is a primary cause of kidney failure globally.
  • Understanding DN pathogenesis is crucial for developing new treatments.

Purpose of the Study:

  • To investigate the role of the lncRNA Dlx6os1/SOX6/EZH2 pathway in diabetic nephropathy progression.
  • To identify potential therapeutic targets for DN.

Main Methods:

  • Quantitative real-time PCR (RT-qPCR) and Western blot to measure gene and protein expression.
  • ELISA for urine microalbumin and blood glucose.
  • RNA immunoprecipitation (RIP) and ChIP-qPCR to confirm molecular interactions.

Main Results:

  • lncRNA Dlx6os1 was upregulated in DN models and high glucose-induced cells.
  • Knockdown of lncRNA Dlx6os1 reduced cell proliferation, fibrosis, and inflammation.
  • lncRNA Dlx6os1 suppressed SOX6 expression by recruiting EZH2, with SOX6 mediating these effects.

Conclusions:

  • lncRNA Dlx6os1 accelerates DN progression.
  • Epigenetic repression of SOX6 via EZH2 recruitment by lncRNA Dlx6os1 is a key mechanism in DN.
Keywords:
Diabetic nephropathyEnhancer of zeste homolog 2LncRNA Dlx6os1SOX6

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