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Updated: Apr 25, 2026

Pre-clinical Evaluation of Tyrosine Kinase Inhibitors for Treatment of Acute Leukemia
Published on: September 18, 2013
[Effect of SU11248 on leukemia cell line K562 and its molecular mechanisms]
Ling-Qing Luo1, Xiao Cheng2, Yan Chen1
1Department of Laboratorial Examination, Fujian Tumor Hospital of Fujian Medical University Teaching Hospital, Fuzhou 350014, Fujian Province, China.
Abstract:
This study was aimed to investigate the effect of SU11248 on proliferation and apoptosis of leukemia cell line K562 in vitro and its mechanism. The inhibitory effect of 3.2 µg/ml SU11248 on K562 proliferation was tested by MTT assay. The ability of SU11248 to induce apoptosis of K562 cells was examined by TUNEL and DNA ladder. The expression of C-MYC, hTERT and BCR-ABL mRNA in K562 cells was detected by RT-PCR. The protein expression of Akt and p-Akt in K562 cells was detected by Western blot. The results showed that the proliferation of K562 cells was obviously inhibited by 3.2 µg/ml SU11248 in a time-dependent manner. SU11248 could induce K562 cells apoptosis in dose-and time-dependent manner. The mRNA expression of C-MYC, hTERT and BCR-ABL was reduced significantly by SU11248 in a time-dependent manner (P < 0.05). Western blot detection showed that the expression of p-Akt protein in K562 cells decreased in dose-and time-dependent manner after SU11248 treatment, but the expression of Akt was not significantly changed. It is concluded that SU11248 can inhibit the growth of K562 cells efficiently through inducing apoptosis, its mechanism may be closely relate with the expression down-regulation of C-MYC, hTERT, BCR-ABL and the inhibition of Akt phosphorylation.
Insights
SU11248 effectively inhibits K562 leukemia cell growth and induces apoptosis. Its mechanism involves down-regulating C-MYC, hTERT, and BCR-ABL mRNA, and inhibiting Akt phosphorylation.
Area of Science:
- Molecular Biology
- Cancer Research
- Pharmacology
Background:
- Leukemia cell line K562 is a model for studying leukemia.
- Understanding the mechanisms of anti-leukemic agents is crucial for treatment development.
Purpose of the Study:
- To investigate the anti-proliferative and pro-apoptotic effects of SU11248 on K562 cells.
- To elucidate the underlying molecular mechanisms of SU11248 action.
Main Methods:
- MTT assay for proliferation.
- TUNEL assay and DNA laddering for apoptosis.
- RT-PCR for mRNA expression (C-MYC, hTERT, BCR-ABL).
- Western blot for protein expression (Akt, p-Akt).
Main Results:
- SU11248 significantly inhibited K562 cell proliferation in a time-dependent manner.
- SU11248 induced apoptosis in K562 cells dose- and time-dependently.
- SU11248 reduced C-MYC, hTERT, and BCR-ABL mRNA levels and inhibited Akt phosphorylation.
Conclusions:
- SU11248 demonstrates potent anti-leukemic activity against K562 cells in vitro.
- The mechanism involves apoptosis induction and downregulation of key oncogenes and signaling pathways.
- SU11248 shows potential as a therapeutic agent for leukemia.
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