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1.
Journal of Experimental Hematology ; (6): 671-676, 2022.
Artículo en Chino | WPRIM | ID: wpr-939674

RESUMEN

OBJECTIVE@#To investigate the effects of paclitaxel, quizartinib and their combination on proliferation, apoptosis and FLT3/STAT5 pathway of human leukemia cell line MV4-11 (FLT3-ITD+).@*METHODS@#MV4-11 cells were treated with paclitaxel and quizartinib at different concentrations for 24 h, 48 h and 72 h, respectively, and then the two drugs were combined at 48 h to compare the inhibition of proliferation, the apoptosis rate was detected by flow cytometry, the expression of FLT3 and STAT5 mRNA was determined by fluorescence quantitative PCR, and the protein expression of FLT3, p-FLT3, STAT5 and p-STAT5 was determined by Western blot.@*RESULTS@#Different combination groups of paclitaxel and quizartinib had synergistic inhibitory effect. The cell survival rate in the combination group was significantly lower than that in the single drug group (P<0.05). The cell apoptosis rate in the combination group was significantly higher than that in the single drug group (P<0.001). The expression of FLT3 mRNA in combination group was significantly higher than that in two single drugs (P<0.01). The expression of STAT5 mRNA in combination group was significantly higher than that in quizartinib group (P<0.001); increased compared with paclitaxel group, but there was no statistical significance. The expression level of p-FLT3、p-STAT5 protein in the combination group was significantly lower than that in the single drug group (P<0.05, P<0.05).@*CONCLUSION@#Paclitaxel combined with quizartinib can synergistically inhibit the proliferation of MV4-11 cell line and promote the apoptosis of MV4-11 cell line by inhibiting the activity of FLT3/STAT5 pathway.


Asunto(s)
Humanos , Apoptosis , Benzotiazoles , Línea Celular Tumoral , Leucemia Mieloide Aguda/genética , Paclitaxel/uso terapéutico , Compuestos de Fenilurea , ARN Mensajero , Factor de Transcripción STAT5/farmacología , Transducción de Señal , Tirosina Quinasa 3 Similar a fms
2.
China Journal of Chinese Materia Medica ; (24): 2116-2119, 2008.
Artículo en Chino | WPRIM | ID: wpr-283782

RESUMEN

<p><b>OBJECTIVE</b>To discuss the anti-tumor activity of ginsenoside Rh2, we observed the expressions of the junction adhesion molecul (JAM) in transplanted-tumor in mice.</p><p><b>METHOD</b>The models of 40 transplanted-tumor mice that were established by subsequently injecting cancer ascite of mice (S180) with 0.2 mL per mouse into the preepipodite skin were divided into two groups. Experiment group was drenched with 2 mL ginsenoside Rh2 per mouse, equating to a dose 20 mg x kg(-1). Control group was drenched with 2 mL normal saline per mouse. The expression of JAM-1, JAM-2 in the lymphatics, blood vessels and tumours were observed by immunohistochemical staining.</p><p><b>RESULT</b>The expression of JAM-1 on the cancer cells was significantly decreased in experiment group (IA 340.55) as compared with control group (IA 549.90, P<0.05). However, JAM-2 weakly expressed in both two groups. The density of blood vessels in which JAM-1, JAM-2 expressed showed 2.33 and 1.34 in control group, and 1.09 and 0.9 in experiment group respectively. Moreove, the density of lymph vessels were respectively 2.23 and 1.88 in control group compared with 0.99 and 0.79 in experiment group. The expression in blood vessels and lymph vessels in control group were significantly higher than those in experiment group, respectively (P<0.05).</p><p><b>CONCLUSION</b>Ginsenoside Rh2 can affect the tumor growth, further angiogenesis and lymphangiogenesis by down-regulating JAM expression in tumor.</p>


Asunto(s)
Animales , Femenino , Masculino , Ratones , Moléculas de Adhesión Celular , Metabolismo , Medicamentos Herbarios Chinos , Farmacología , Regulación de la Expresión Génica , Ginsenósidos , Farmacología , Inmunoglobulinas , Metabolismo , Inmunohistoquímica , Trasplante de Neoplasias , Neoplasias , Metabolismo , Patología , Receptores de Superficie Celular , Metabolismo
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