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Linc01271 promotes lipid synthesis and MASLD/MASH progression via miR-149-3p/RAB35 axis

Zhaoqing Yin1,2, Caibin Yue3,4, Zhipeng Li1,2

  • 1Department of Hepatobiliary Surgery, The Second Hospital of Shandong University, Jinan, China.

Cellular and Molecular Life Sciences : CMLS
|September 8, 2025
PubMed

Insights

Long non-coding RNA Linc01271 promotes metabolic associated steatohepatitis (MASH) by increasing lipid synthesis and inflammation. Targeting Linc01271 may offer a new therapeutic strategy for MASH.

Area of Science:

  • Hepatology
  • Molecular Biology
  • Genetics

Background:

  • Metabolic associated steatohepatitis (MASH) is a severe liver condition linked to metabolic dysfunction.
  • The precise molecular drivers of MASH progression are not fully understood.
  • Identifying novel molecular targets is crucial for developing effective MASH therapies.

Purpose of the Study:

  • To investigate the role of long non-coding RNA Linc01271 in the pathogenesis of MASH.
  • To elucidate the molecular mechanisms involving the miR-149-3p/RAB35 axis and PI3K/AKT/mTOR pathway in MASH.
  • To assess Linc01271 as a potential therapeutic target for MASH.

Main Methods:

  • Transcriptome sequencing and RT-qPCR to analyze Linc01271 expression in MASH tissues.
  • In vitro experiments using THLE-2 cells to assess the effects of Linc01271 knockdown or overexpression on lipid metabolism and inflammation.
  • Dual-luciferase reporter assays to confirm interactions between Linc01271 and miR-149-3p.
  • In vivo studies in mice to evaluate the impact of Linc01271 knockdown on MASH progression.

Main Results:

  • Linc01271 was significantly upregulated in MASH tissues, correlating with increased lipid accumulation and inflammation.
  • Linc01271 knockdown in cells reduced lipid synthesis and pro-inflammatory cytokine expression.
  • Linc01271 was confirmed to interact with miR-149-3p, influencing the regulation of RAB35.
  • Linc01271 knockdown in mice ameliorated MASH, reducing liver injury and metabolic dysfunction markers.

Conclusions:

  • Linc01271 promotes MASH by enhancing lipid synthesis and inflammatory responses via the miR-149-3p/RAB35 axis and PI3K/AKT/mTOR pathway.
  • Linc01271 represents a promising therapeutic target for MASLD/MASH.
  • Further investigation is needed to develop Linc01271-targeted therapies for clinical application.
Keywords:
Linc01271Lipid metabolismMASHMASLDMiR-149-3pRAB35

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