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Related Experiment Video

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Drug Repurposing Hypothesis Generation Using the "RE:fine Drugs" System
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Transcriptome-Guided Drug Repurposing Identifies Homoharringtonine (HHT) as a Candidate for Radiation-Induced

Mohamed El-Agamy Farh1,2,3, Sang Yeon Kim1,4, Sunjoo Park1

  • 1Department of Radiation Oncology, College of Medicine, Yonsei University, Seoul 03722, Republic of Korea.

Pharmaceutics
|December 31, 2025
PubMed
Summary

Homoharringtonine (HHT) shows promise in treating radiation-induced pulmonary fibrosis (RPF) by inhibiting protein synthesis and key fibrotic pathways. This drug repurposing approach offers a novel therapeutic strategy for RPF patients.

Keywords:
LINCSREMEDYRhoA/ROCKWnt/β-catenindrug repurposinghomoharringtonineradiation-induced pulmonary fibrosis

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Area of Science:

  • Pulmonary Medicine
  • Oncology
  • Pharmacology

Background:

  • Radiation-induced pulmonary fibrosis (RPF) is a significant complication of lung cancer radiotherapy with limited treatment options.
  • Existing therapies for RPF are scarce, necessitating the exploration of novel therapeutic strategies.

Purpose of the Study:

  • To identify potential drug candidates for RPF through a transcriptome-based drug repurposing approach.
  • To investigate the anti-fibrotic effects and underlying mechanisms of homoharringtonine (HHT) in RPF.

Main Methods:

  • Utilized the REMEDY computational platform and LINCS database for transcriptome-based drug repurposing.
  • Employed an in vitro fibrotic model using activated MRC-5 human lung fibroblasts to assess HHT's anti-fibrotic effects.
  • Conducted in silico molecular docking to explore HHT's interaction with fibrosis-related targets.

Main Results:

  • HHT significantly reduced fibroblast proliferation, myofibroblast differentiation, and extracellular matrix production in vitro.
  • HHT suppressed key fibrotic markers, including cyclin D1, α-smooth muscle actin (α-SMA), and collagen deposition.
  • Mechanistic studies revealed HHT modulates RhoA/ROCK and Wnt/β-catenin signaling pathways, with potential direct interaction with integrins and Frizzled receptors.

Conclusions:

  • Homoharringtonine (HHT) demonstrates potential as a therapeutic agent for radiation-induced pulmonary fibrosis (RPF).
  • HHT exhibits a dual mechanism of action, inhibiting protein synthesis and specific fibrotic signaling pathways.
  • This study validates the use of computational drug repurposing for RPF and warrants further preclinical investigation of HHT.