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Dieckol prevents prostate cancer cell proliferation by transcriptionally attenuating JAK/STAT3 signaling pathway

Vimala Karuppaiya1, Asaikkutti Annamalai2, Shanthi Krishnamurthy3

  • 1Division of Cancer Nanomedicine, Department of Zoology, Periyar University, Salem, India.

Environmental Toxicology
|October 27, 2023
PubMed

Insights

Dieckol (DCL), a natural compound, inhibits prostate cancer cell growth and migration by blocking the JAK/STAT3 pathway. DCL demonstrates chemotherapeutic potential by inducing apoptosis and reducing proliferation-related proteins.

Area of Science:

  • Biochemistry
  • Molecular Biology
  • Cancer Research

Background:

  • Prostate cancer remains a leading cause of cancer-related deaths globally.
  • Targeting specific signaling pathways offers a promising strategy for novel cancer therapies.
  • The JAK/STAT3 pathway is frequently implicated in prostate cancer progression.

Purpose of the Study:

  • To investigate the anti-cancer effects of dieckol (DCL) on human prostate cancer PC-3 cells.
  • To elucidate the underlying molecular mechanisms, focusing on the JAK/STAT3 signaling pathway.

Main Methods:

  • PC-3 cells were treated with varying concentrations of DCL (0-20 μM) for 24 hours.
  • Cytotoxicity assessed via MTT assay; ROS generation measured by DCFH-DA staining.
  • Apoptosis and mitochondrial membrane potential (MMP) evaluated using AO/EtBr and fluorescent staining.
  • Protein expression analysis conducted through flow cytometry and Western blotting.

Main Results:

  • DCL exhibited significant cytotoxicity against PC-3 cells with an IC50 of 12 μM.
  • DCL treatment induced significant reactive oxygen species (ROS) generation and apoptosis.
  • DCL suppressed key proteins in the JAK/STAT3 pathway (STAT3, JAK1) and proliferation markers (PCNA, cyclins D1/E1).
  • DCL upregulated pro-apoptotic proteins (Bax, caspase-3, cytochrome C) and decreased MMP.

Conclusions:

  • Dieckol effectively inhibits prostate cancer cell proliferation and migration.
  • DCL exerts its anti-cancer effects by inhibiting the JAK/STAT3 pathway and inducing apoptosis.
  • DCL shows potential as a chemotherapeutic agent for prostate cancer treatment.
Keywords:
JAK/STAT3 signaling pathwayapoptosisdieckolproliferationprostate cancer

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