2. Academic Validation
  3. SNAI1-activated long non-coding RNA LINC01711 promotes hepatic fibrosis cell proliferation and migration by regulating XYLT1

SNAI1-activated long non-coding RNA LINC01711 promotes hepatic fibrosis cell proliferation and migration by regulating XYLT1

  • Genomics. 2023 Mar 3;110597. doi: 10.1016/j.ygeno.2023.110597.
Linan Bao 1,  Yang Chu 1,  Hui Kang 2
Affiliations

Affiliations

  • 1 Department of Laboratory Medicine, The First Affiliated Hospital of China Medical University, Shenyang 110001, Liaoning Province, China.
  • 2 Department of Laboratory Medicine, The First Affiliated Hospital of China Medical University, Shenyang 110001, Liaoning Province, China. Electronic address: kanghui@cmu.edu.cn.
PMID: 36871637 DOI: 10.1016/j.ygeno.2023.110597
Abstract

Liver fibrosis is the result of the accumulation of extracellular matrix (ECM) that cannot be cleared. Bioinformatic analysis showed that LINC01711 was significantly overexpressed in hepatic fibrosis. The regulatory mechanism of LINC01711 was clarified and confirmed the transcription factors associated with LINC01711. Functionally, LINC01711 promoted LX-2 cell proliferation and migration, indicating that it exerts effects promoting the progression of hepatic fibrosis. Mechanistically, LINC01711 increased the expression of xylosyltransferase 1 (XYLT1), which is an important protein for constructing the ECM. We also confirmed that SNAI1 activated LINC01711 transcription. Taking these findings together, LINC01711 was induced by SNAI1 and promoted the proliferation and migration of LX-2 cells via XYLT1. This study will help to understand the function of LINC01711 and its regulatory mechanism in hepatic fibrosis.

Keywords

Hepatic fibrosis; Long non-coding RNA (lncRNA); Xylosyltransferase 1 (XYLT1).

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