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Updated: May 6, 2026

Pre-clinical Evaluation of Tyrosine Kinase Inhibitors for Treatment of Acute Leukemia
10:49

Pre-clinical Evaluation of Tyrosine Kinase Inhibitors for Treatment of Acute Leukemia

Published on: September 18, 2013

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[Triptolide inhibits proliferation and induces apoptosis of imatinib resistant K562/G01 cells]

Si-Qun Wen1, Liang-Ming Ma, Yu-Jin Lu

  • 1Department of Hematology, Shangxi Big Hospital of Shangxi Medical University, Taiyuan 030032, Shangxi Province, China.

Zhongguo Shi Yan Xue Ye Xue Za Zhi
|October 26, 2013
PubMed

Insights

Triptolide enhances imatinib

Area of Science:

  • Pharmacology
  • Molecular Biology
  • Cancer Research

Background:

  • K562/G01 cells are a model for drug-resistant leukemia.
  • Imatinib is a standard treatment, but resistance can develop.
  • Novel therapeutic strategies are needed to overcome drug resistance.

Purpose of the Study:

  • To investigate triptolide's inhibitory effect on K562/G01 cell proliferation.
  • To explore triptolide's role in inducing apoptosis in K562/G01 cells.
  • To elucidate the underlying mechanisms of triptolide's action.

Main Methods:

  • MTT assay for proliferation.
  • Flow cytometry (FCM) for cell cycle and apoptosis.
  • Western blot for P-glycoprotein (P-gp) expression.
  • Real-time quantitative PCR for BCR/ABL gene expression.

Main Results:

  • Triptolide enhanced imatinib's inhibitory effect on K562/G01 proliferation and apoptosis.
  • Triptolide induced G1 phase cell cycle arrest.
  • Triptolide down-regulated BCR/ABL gene and P-gp protein expression.

Conclusions:

  • Triptolide exhibits anti-proliferative and pro-apoptotic effects on K562/G01 cells.
  • Mechanisms involve cell cycle arrest, reduced P-gp expression, and inhibited BCR/ABL gene expression.
  • Triptolide shows potential as an adjuvant therapy for imatinib-resistant leukemia.

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