Long non-coding RNA MIR22HG impedes the progression of anaplastic thyroid carcinoma via targeting miR-141-3p/PTEN/AKT

Junyu Cao1, Peng Jiang2, Songliang Jiang2

  • 1Department of Breast and Thyroid Surgery, The First People's Hospital of Yunnan Province, The Affiliated Hospital of Kunming University of Science and Technology, Kunming, Yunnan, China. junyucao@kust.edu.cn.

PubMed
Abstract

Insights

The long non-coding RNA MIR22HG acts as a tumor suppressor in anaplastic thyroid carcinoma (ATC). Its downregulation promotes ATC progression by affecting the miR-141-3p/PTEN/AKT pathway, offering new therapeutic targets.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Anaplastic thyroid carcinoma (ATC) is a highly aggressive and lethal cancer.
  • The long non-coding RNA MIR22HG is implicated in various cancers, but its role in ATC is unclear.

Purpose of the Study:

  • To investigate the function and molecular mechanisms of MIR22HG in anaplastic thyroid carcinoma.
  • To explore MIR22HG as a potential therapeutic target for ATC.

Main Methods:

  • Quantitative real-time PCR (qRT-PCR) to assess MIR22HG expression.
  • In vitro and in vivo assays (MTT, wound healing, Matrigel invasion) to evaluate cell proliferation and metastasis.
  • RNA immunoprecipitation (RIP), RNA pull-down, and dual-luciferase reporter assays to elucidate molecular interactions.

Main Results:

  • MIR22HG expression was significantly downregulated in ATC tissues and cells.
  • Lower MIR22HG levels correlated with poorer prognosis in ATC patients.
  • Overexpression of MIR22HG suppressed ATC cell proliferation and metastasis.
  • MIR22HG positively regulated PTEN by sponging miR-141-3p, inhibiting the AKT signaling pathway.

Conclusions:

  • MIR22HG functions as a tumor suppressor in ATC.
  • The MIR22HG/miR-141-3p/PTEN/AKT axis is critical in ATC progression.
  • Targeting this axis may offer novel therapeutic strategies for ATC.

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