RESUMEN
<p><b>OBJECTIVE</b>To explore the mechanism of matrine (Mat) induced human erythroleukemia TF-1 cell apoptosis and its effect on SALL4 expression.</p><p><b>METHOD</b>Different concentrations of the Mat (0.5, 1.0, 1.5, 2.0 g x L(-1) ) were cultured in vitro in TF-1 cells at different time (24, 48, 72 h). Cell proliferation was assayed by MTT. Cell cycle was determined by flow cytometry (FCM). Cell apoptosis was detected by Annexin V and PI double staining method. SALL4 mRNA expression was detected by reverse transcription RT-PCR (RTT-PCR).</p><p><b>RESULT</b>Administrated with Mat (0.5-2.0 g x L(-1)) after 24, 48, 72 h, the proliferation of TF-1 cells were inhibited (P < 0.01) , and in dose- and time-dependent manner. Half inhibitory concentration (IC50 ) was 1.0 g L(-1) at 48 h. After 48 h that the Mat acted on TF-1 cells, the proportion of G0/G1 phase cells increased while compared with the control group, and S phase cells decreased (P < 0.01). Apoptosis were 8.6% , 11.21%, 15.26% , 17.63%, which showed statistically significant difference (P < 0.01) compared with the control group (5.05%). RT-PCR results showed the ratio between SALL4 mRNA expression and beta-actin (internal reference) expression significantly decreased (P < 0.01) with Mat dose increased.</p><p><b>CONCLUSION</b>In a certain range of concentration and time, Mat can inhibit TFT-1 cells proliferation. The mechanism is to make the cells G0/G1 phase blocked, to inhibit SALL4 gene expression and induce cell apoptosis.</p>
Asunto(s)
Humanos , Alcaloides , Farmacología , Antineoplásicos Fitogénicos , Farmacología , Apoptosis , Ciclo Celular , Línea Celular Tumoral , Proliferación Celular , Expresión Génica , Leucemia Eritroblástica Aguda , Quimioterapia , Genética , Metabolismo , Quinolizinas , Farmacología , Factores de Transcripción , Genética , MetabolismoRESUMEN
SALL4 gene is closely related to body malformations related diseases, embryonic stem cell development, and hematopoietic malignancies. SALL4 can activate hematopoietic stem cell through Wnt signaling pathways, and promote continued proliferation of leukemia stem cells, leading to leukemia. In-depth study of SALL4 gene and its protein function will help clarify the pathogenesis of leukemia, providing a new target for the treatment of leukemia.