AI Article Synopsis
- - The study examined how cinnamic aldehyde (CA) affects apoptosis in chronic myeloid leukemia (CML) cells using K562 cell lines and bone marrow samples from CML patients.
- - Various concentrations of CA were tested, revealing that it triggered apoptosis in K562 cells and CML bone marrow mononuclear cells in a dose- and time-dependent manner.
- - The findings showed that CA decreased levels of BCR-ABL mRNA and C-MYC protein while also reducing phosphorylation of CrkL, suggesting that the down-regulation of these factors is a key mechanism for CA's anti-leukemia effects.
Article Abstract
The aim of this study was to investigate the apoptosis-inducing effect of cinnamic aldehyde (CA) on chronic myeloid leukemic (CML) cells and its mechanism. K562 cells and primary bone marrow mononuclear cells (MNC) from patients with CML were treated by various concentrations of CA. Flow cytometry was employed to measure the apoptosis of K562 cells and primary CML bone marrow MNC. Western blot was used to determine the expression of C-MYC and the phosphorylation of CrkL in K562 cells, and real-time polymerase chain reaction (real-time PCR) was used to quantify the expression of BCR-ABL mRNA in K562 cells. The results indicated that CA induced the apoptosis of K562 cells in a time- and dose-dependent manner. CA induced apoptosis of CML MNC dose-dependently. CA inhibited the expression of BCR-ABL mRNA and C-MYC, reduced CrkL phosphorylation levels in K562 cells. It is concluded that CA induces apoptosis of CML cells in vitro. Down-regulation of the expression and function of BCR-ABL may be one of its most important anti-leukemia mechanisms.
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