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Dieckol induces cell cycle arrest by down-regulating CDK2/cyclin E in response to p21/p53 activation in human

Seong-Yeong Heo1,2,3, Min-Seon Jeong4, Hyoung Shin Lee5

  • 1Research Center for Marine Integrated Bionics Technology, Pukyong National University, Busan, Republic of Korea.

Cell Biochemistry and Function
|October 28, 2021
PubMed

Insights

Dieckol, derived from Ecklonia cava, effectively inhibits human tracheal fibroblast proliferation. It induces cell cycle arrest by modulating key proteins, suggesting therapeutic potential for fibrotic conditions.

Area of Science:

  • Marine Natural Products Chemistry
  • Cell Biology
  • Molecular Pharmacology

Background:

  • Dieckol, a phlorotannin from Ecklonia cava, possesses known anti-inflammatory, anti-bacterial, anti-oxidative, anti-adipogenic, and anti-stenosis properties.
  • The specific role of dieckol in regulating cyclin-dependent kinase 2 (CDK2)/cyclin E signaling, a critical pathway in fibrosis development, remains unelucidated.

Purpose of the Study:

  • To investigate the effect of dieckol on cell proliferation and cell cycle regulation in human tracheal fibroblasts (Hs680.Tr).
  • To elucidate the molecular mechanisms underlying dieckol's action, particularly its interaction with CDK2/cyclin E signaling pathways.

Main Methods:

  • Isolation and purification of dieckol from Ecklonia cava.
  • Assessment of dieckol's anti-proliferative activity on Hs680.Tr fibroblasts.
  • Western blotting to analyze the expression of cell cycle regulatory proteins (CDK2, cyclin E, p21, p53).
  • Molecular docking studies to predict dieckol's interaction with transforming growth factor-β receptor.

Main Results:

  • Dieckol demonstrated significant anti-proliferative effects on Hs680.Tr human tracheal fibroblasts.
  • Dieckol induced G0/G1 phase cell cycle arrest in a dose-dependent manner.
  • This arrest was associated with the downregulation of CDK2 and cyclin E, and the upregulation of p21 and p53.
  • Molecular docking indicated high-affinity binding of dieckol to transforming growth factor-β receptor.

Conclusions:

  • Dieckol effectively inhibits the proliferation of Hs680.Tr human tracheal fibroblasts.
  • The anti-proliferative mechanism involves G0/G1 cell cycle arrest mediated by p21 and p53.
  • Dieckol's interaction with TGF-β receptor suggests a potential role in fibrotic pathway regulation.
Keywords:
DieckolEcklonia cavacell cycle arrestcyclin E/CDK2 complexhuman tracheal fibroblasts

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