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Updated: Dec 23, 2025

Identification of Mediators of T-cell Receptor Signaling via the Screening of Chemical Inhibitor Libraries
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Identification of Mediators of T-cell Receptor Signaling via the Screening of Chemical Inhibitor Libraries

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[Costunolide Suppresses Proliferation of K562 Cells through JAK/STAT Signaling Pathway]

Jie Jiang1, Hong Cai1, Jie Qu2

  • 1Department of Clinical Laboratorial Examination, The Second Hospital Affiliated to Dalian Medical University, Dalian 116023, Liaoning Province, China.

Zhongguo Shi Yan Xue Ye Xue Za Zhi
|April 23, 2020
PubMed
Abstract

Insights

Costunolide inhibits chronic myeloid leukemia K562 cell proliferation by inducing apoptosis and increasing reactive oxygen species (ROS). This natural compound targets the JAK/STAT signaling pathway, offering potential therapeutic strategies.

Area of Science:

  • Oncology
  • Molecular Biology
  • Pharmacology

Background:

  • Chronic myeloid leukemia (CML) is a myeloproliferative neoplasm.
  • K562 is a human CML cell line frequently used in leukemia research.
  • Identifying novel therapeutic agents for CML is crucial.

Purpose of the Study:

  • To investigate the anti-proliferative effects of costunolide on K562 cells.
  • To elucidate the underlying molecular mechanisms, including apoptosis and signaling pathways.

Main Methods:

  • Cell viability assessed using CCK-8 assay.
  • Apoptosis and reactive oxygen species (ROS) levels measured by flow cytometry.
  • Protein expression analyzed via Western blot.

Main Results:

  • Costunolide significantly inhibited K562 cell proliferation with an IC50 of approximately 15.70 μmol/L.
  • Costunolide induced significant apoptosis and increased ROS levels in K562 cells.
  • Inhibition of p-JAK2, p-STAT3, and BCL-2, with increased BAX, cytochrome C, cleaved-caspase-3, and cleaved-PARP expression observed.

Conclusions:

  • Costunolide effectively suppresses K562 cell proliferation.
  • The mechanism involves the induction of apoptosis and ROS generation via the JAK/STAT signaling pathway.

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