The Mechanism Of Aapoptosis Of K562 Tumor Cell Line Induced By ABPS

Purpose: Study the mechanism of tumor cell's apoptosis induced by Agaricus blazei Polysaccharid (ABPS), and the effect of P53, Caspase-3 and P16 genes in this inducing process otherwise. Method: We use Methyl Thiazolyl Tetrazolium (MTT) colorimetric and Colony Formaing method to observate the effect of growth inhibiting and cell multiplication of K562 tumor cell induced by ABPS, and flow cytometer , tansmission electron microscope(TEM), Fluorescence microscope (FCM) and DNA gel-electrophoretic apparatus also was used to test the occurrence of K562 tumor cell's apoptosis induced by ABPS. And we used Reverse Transcription-Polymerase Chain Reacton(RT-PCR) to detect the expression of Caspase-3, p53 and P16 genes in this apoptosis. Result: 1 Agaricus blazei Polysaccharid can induce K562 tumor cell's apoptosis, we can see typical morphologic change of apoptosis cells: karyopyknosis, chromatin's condensing and aggregation in nuclear, forming crescent-shaped or annulus structures to lean on edge of cell nucleus's membrane and posing apoptosis body also. FCM can detect visible hypodiploid capylus of K562 tumor cell induced by 1mg/ml ABPS. And there was significant difference compared with control group (p< 0.01 ) , inhibition ratio had significant positive correlation with medication dosage and time(r=0.875); during 0~1mg/ml dosage amplitude, inhibition ratio accrescenced by dosage's increasing. However, the inhibition ratio would decrease when dosage over 10mg/ml.3 ABPS can enhance Caspase-3, p53 an P16 genes' expression activity, evoke DNA's degradation an damage, down-regulate cell's generation cycle activity to urge cells ingress G1 stage from G0 stage, to inhibittumor cell's growth. Conclusion: ABPS can inhibit K562 tumor cell's growth and generation, and induce apoptosis likewise by up-regulating Caspase-3, p53 and P16 genes' expression.