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In Vivo Inhibition of MicroRNA to Decrease Tumor Growth in Mice
07:02

In Vivo Inhibition of MicroRNA to Decrease Tumor Growth in Mice

Published on: August 23, 2019

Downregulation of microRNAs directs the EMT and invasive potential of anaplastic thyroid carcinomas

J Braun1, C Hoang-Vu, H Dralle

  • 1Department of Molecular Cell Biology, Martin Luther University Halle-Wittenberg, Halle, Germany.

Oncogene
|May 26, 2010
PubMed

Insights

Anaplastic thyroid carcinomas (ATCs) show distinct microRNA patterns, with decreased miR-200 and miR-30 families. Inhibiting TGFBR1 may treat ATCs by inducing epithelial transition and reducing invasion.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Anaplastic thyroid carcinomas (ATCs) are aggressive tumors originating from thyroid epithelial cells via mesenchymal transition.
  • Specific microRNA (miRNA) signatures may differentiate ATCs from other thyroid cancers, but their role in de-/transdifferentiation and invasion is unclear.

Purpose of the Study:

  • To identify distinct miRNA patterns in ATCs associated with mesenchymal de-/transdifferentiation and invasion.
  • To investigate the functional role of specific miRNAs and transforming growth factor (TGF)beta signaling in ATC progression and potential therapeutic targets.

Main Methods:

  • Differential expression analysis of miRNAs in ATCs compared to follicular thyroid carcinomas.
  • Functional studies involving miRNA expression modulation in ATC-derived cells to assess effects on invasion and epithelial-mesenchymal transition (EMT).
  • Analysis of TGF-beta signaling pathway components (SMAD2, TGFBR1) and their regulation by miRNAs.

Main Results:

  • Two miRNA families, miR-200 and miR-30, were significantly decreased in ATCs and distinguished them from papillary and follicular thyroid carcinomas.
  • Restoring miR-200 and miR-30 expression in ATC cells reduced invasiveness and induced mesenchymal-epithelial transition (MET).
  • TGF-beta signaling components (SMAD2, TGFBR1), upregulated in ATCs, were regulated by miR-30 and/or miR-200. TGFBR1 inhibition induced MET and reduced miR-21 while increasing miR-200.

Conclusions:

  • Altered miRNA signatures, specifically decreased miR-200 and miR-30, are potent markers for ATCs and are linked to EMT and invasion.
  • TGFBR1 inhibition shows therapeutic potential for ATCs by promoting MET, reducing invasion, and modulating miRNA expression.

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