RESUMEN
To investigate the effect of apigenin on self-renewal for sphere-forming cells in human small cell lung cancer cell line NCI-H446 and the underlying mechanisms. Methods: Sphere-forming cells from NCI-H446 cell line were cultured in stem cell-conditioned culture medium with ultra-low attachment surface plates. The rate of sphere-forming cells in the second passage sphere-forming cells was used to evaluate the inhibitory effects of apigenin on the self-renewal for sphere-forming cells. The protein level of urokinase-type plasminogen activator receptor (uPAR) in spheroids was analyzed by Western blot. Results: Apigenin signifcantly inhibited the self-renewal of the second passage sphere-forming cells [0, 5.0, 10.0, 20.0 μmol/L apigenin: (18.2±1.9)%, (13.6±1.7)%, (10.6±1.6)%, (6.9±1.3)%, respectively] and down-regulated uPAR expression in a concentration-dependent manner (P<0.05). Conclusion: Apigenin inhibits the self-renewal capacity of sphere-forming cells in NCI-H446 cells, which may be associated with down-regulation of uPAR expression.
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Humanos , Apigenina , Farmacología , Línea Celular Tumoral , Regulación hacia Abajo , Genética , Neoplasias Pulmonares , Células Madre Neoplásicas , Patología , Fisiología , Receptores de Superficie Celular , Receptores del Activador de Plasminógeno Tipo Uroquinasa , Genética , Metabolismo , Transducción de Señal , Carcinoma Pulmonar de Células Pequeñas , Quimioterapia , Patología , Esferoides Celulares , Fisiología , Células MadreRESUMEN
Objective To investigate the roles of TLR3 pathway activiated by polyI:C in proliferation and apoptosis of multiple myeloma (MM) RPMI8226 cell line.Methods RPMI8226 cells were cultured in RPMI 1640 with different dose of polyl:C.Cells were collected in different time.Proliferation and apoptosis were detected by CCK-8 kit and flow cytometry,separately.Results The proliferation of RPM18226 was inhibited by polyI:C,and it was dose and time dependent,24 h:12.30％ ±2.04％,22.50％±2.20％,37.90％ ±1.30％ ; 48 h:17.80％ ±1.52％,29.60％ ±0.85％,45.80％ ±1.68％ ;72 h:25.10％±1.01％,34.60％±1.27％,60.50％±2.08％,P＜0.05.RPMI8226 cells were incubated with 50 μg/ml,100 μg/ml and 200 μg/ml polyI:C for 48 h.Apoptotic rate were 5.60％ ±1.06％,8.71％ ±1.06％ and 13.93％ ±1.17％,P＜0.05.TLR3 and TRIF mRNA expression increased obviously and dose dependent,TLR3:1.41±0.10,2.24±0.16,4.08±0.13; TRIF:1.07±0.16,1.97±0.13,3.56±0.19,P＜0.05.Conclusion The proliferation of MM cells were inhibited by TLR3 pathway obviously,and apoptosis was induced by polyI:C.
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OBJECTIVE To study the existence of integron and metallo-?-lactamase in Stenotrophomonas maltophilia in our hospital.METHODS The antibiotic susceptibility was tested by K-B method.The genomic DNA and their plasmids were extracted.The integron and metallo-?-lactamase gene were amplified by polymerase chain reaction(PCR).RESULTS L1 and L2 genes were amplified in chromosomes and plasmids.Integrons Ⅰ and Ⅱ were detected in genomic DNA.CONCLUSIONS Existence of metallo-?-lactamase is one of reasons of multi-drug resistance in S.maltophilia.S.maltophilia can receive integrons and gain its multi-drug resistance from other strains.