Related Experiment Video

Updated: Jun 9, 2025

Isolation, Culture, and Characterization of Primary Dermal Fibroblasts from Human Keloid Tissue
04:41

Isolation, Culture, and Characterization of Primary Dermal Fibroblasts from Human Keloid Tissue

Published on: July 28, 2023

2.1K

Genistein inhibited endocytosis and fibrogenesis in keloid via CTGF signaling pathways

Chun-Te Lu1,2, Jiunn-Liang Ko3,4, Chu-Chyn Ou5,6

  • 1Division of Plastic and Reconstructive Surgery, Department of Surgery, Taichung Veterans General Hospital, Taichung, 407, Taiwan.

Genes & Nutrition
|October 28, 2024
PubMed
Abstract

Insights

Genistein, a soy isoflavone, effectively inhibits keloid fibroblast cell migration and proliferation by inducing cell cycle arrest via the CTGF pathway. This research offers a novel therapeutic strategy for keloid treatment.

Area of Science:

  • Biochemistry
  • Dermatology
  • Cell Biology

Background:

  • Keloids are abnormal scars resulting from excessive fibroblast activity.
  • Soy isoflavones, particularly genistein, are investigated for their therapeutic potential.
  • Human keloid fibroblast cells (KFs) and tissue models are used to study keloid pathogenesis.

Purpose of the Study:

  • To evaluate the effects of genistein on keloid fibroblast cells and tissue.
  • To investigate genistein's mechanism of action in keloid treatment.
  • To explore genistein as a potential therapeutic agent for keloids.

Main Methods:

  • Cell migration assays (wound-healing) were performed.
  • Apoptosis was measured using flow cytometry.
  • Protein and mRNA expression (COL1A1, FN, CTGF, p53) were analyzed via Western blotting and immunofluorescence.
  • Connective tissue growth factor (CTGF) knockdown was utilized.

Main Results:

  • Genistein suppressed KF proliferation and migration, inducing G2/M cell cycle arrest and upregulating p53.
  • Genistein inhibited COL1A1, FN, and CTGF expression.
  • CTGF knockdown reduced KF migration.
  • Genistein mitigated TGF-β1-induced fibrosis and reduced cell migration in a time- and dose-dependent manner.

Conclusions:

  • Genistein-induced p53 triggers cell cycle arrest through the CTGF pathway, inhibiting keloid cell proliferation.
  • Genistein effectively suppresses keloid cell migration.
  • This study presents genistein as a promising therapeutic strategy for keloid treatment.
Keywords:
CTGFCollagenFibronectinGenisteinKeloid

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