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RETRACTED: Gravina et al. The Brain Penetrating and Dual TORC1/TORC2 Inhibitor, RES529, Elicits Anti-Glioma Activity and Enhances the Therapeutic Effects of Anti-Angiogenetic Compounds in Preclinical Murine Models. <i>Cancers</i> 2019, <i>11</i>, 1604.

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The Novel mTOR Complex 1/2 Inhibitor P529 Inhibits Human Lung Myofibroblast Differentiation.

Keith T Ferguson1, Elizabeth E Torr1, Ksenija Bernau1

  • 1Division of Allergy, Pulmonary, and Critical Care Medicine, University of Wisconsin-Madison School of Medicine and Public Health, 600 Highland Ave, Madison, Wisconsin, 53792.

Journal of Cellular Biochemistry
|January 13, 2017
PubMed
Summary

Palomid 529 (P529), a novel mTORC1/2 inhibitor, effectively reduces TGF-β-induced myofibroblast differentiation and extracellular matrix production in lung fibroblasts. This suggests P529 is a promising therapeutic candidate for treating fibrotic lung diseases.

Keywords:
ACTIN CYTOSKELETONFIBRONECTIN DEPOSITIONMYOFIBROBLASTP529PULMONARY FIBROSISSmadTGF-βmTORmTORC1mTORC2

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Area of Science:

  • Cell Biology
  • Pharmacology
  • Pulmonary Medicine

Background:

  • Idiopathic pulmonary fibrosis (IPF) is a progressive, fatal lung disease with limited treatment options.
  • Mechanistic target of rapamycin (mTOR) signaling pathways are implicated in fibrotic processes.
  • Palomid 529 (P529) is a novel dual inhibitor of mTOR complex 1/2 (mTORC1/2).

Purpose of the Study:

  • To investigate the effects of P529 on transforming growth factor-beta (TGF-β)-dependent signaling.
  • To determine P529's impact on myofibroblast differentiation and extracellular matrix production in lung fibroblasts.

Main Methods:

  • Human lung fibroblasts were treated with P529 and TGF-β.
  • Assessed phosphorylation of mTORC1 (p70 S6 kinase 1, 4E-BP1) and mTORC2 (Akt) targets.
  • Evaluated TGF-β-induced myofibroblast differentiation, fibronectin and collagen expression, and Smad signaling.

Main Results:

  • P529 dose-dependently inhibited TGF-β-induced phosphorylation of mTORC1 and mTORC2 targets.
  • P529 significantly reduced TGF-β-induced myofibroblast differentiation, collagen and fibronectin expression, and actin stress fiber formation.
  • P529 did not affect canonical Smad signaling but mTORC1/2 activation was dependent on TGF-β type I receptor (ALK5) and Smad2/3.

Conclusions:

  • P529 effectively inhibits TGF-β-induced myofibroblast differentiation and matrix deposition in lung fibroblasts.
  • Inhibition of mTORC1/2 by P529 disrupts key fibrotic signaling pathways.
  • P529 represents a potential therapeutic strategy for inhibiting in vivo fibrosis.