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Aim To explore the effects of ophiopogo-nin-B (OP-B)on cell cycle and mitosis in non-small cell lung cancer (NSCLC)H460 cells in vitro and the underlying mechanisms. Methods TUNEL immuno-histochemical assay was used to detect the change of the nuclear matter. DAPI staining was used to detect the change of the nuclear morphology and the mitosis status. Meanwhile,Western blot was performed to de-termine the protein level of the proteins regulating cell cycle and mitosis. Results OP-B significantly arres-ted cell cycle in G0 / G1 phase and inhibited the mitosis in H460 cells at the concentration of 10 μmol·L - 1 . Meanwhile,it inhibited the protein level of cyclinD1, cyclinB1,and up-regulated the expression of Myt and the phosphorylation level of Cdc2. Conclusion OP-B inhibits cell mitosis in A549 cells through Myt/ Cdc2 signaling pathway.
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Aims Toevaluatethepharmacodynamic efficacy of different types of antiangiogenic agents as HM-3 on a non-small cell lung cancer xenografts tumor model .To explore the interaction between the antian-giogenic agents and the tumor microenvironment,and to offer suggestions for clinical therapy.Methods Thenon-smallcelllungcarcinomaxenograftmodelwas established in Balb/c nude mice.The model mice were treated with Docetaxel(10 mg·kg-1 )as the positive control.The mice were parallelly treated with,HM-3 at the doses of 3 mg · kg-1 and 48 mg · kg-1 and, Avastin(5 mg·kg-1 ).The parameters include tumor volume,tumor weight and immunohistochemical analy-sis.Result Animalexperimentsshowedthatdocetaxel had good anti-tumor activity.Tumor growth inhibition by tumor weight of G2 docetaxel(10 mg·kg-1 )group was 60. 80%.Tumor growth inhibition by tumor weight of G3 HM-3(3 mg·kg-1 )group,G4 HM-3(48 mg· kg-1 )group ,G4 Avastin(5 mg·kg-1 )group,were 43. 60%,-34. 80%,44. 40%,respectively.Con-clusion Theantigiogeniceffectisaffectedbytumor growth stage,tumor microenvironment and their work-ing mechanisms.Angiogenesis inhibitors HM-3 has a certain effect of inhibiting tumor growth,but to little a-vail.HM-3 shows on inhibitory effect in a dose-de-pendent manner at the doses of 0~6 mg·kg-1 .HM-3 at a high dose of 48 mg · kg-1 has no inhibitory but promoting effects on human non-small cell lung carci-noma A549 xenografts in nude mice .Special dose-effect relationship indicates that dosage should be paid attention to in the clinical use of blood vessel inhibi-tors.
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Objective To investigate the clinical efficacy and side reaction of brucea javanica oil ( BJO) combined with 125I and chemotherapy on stageⅢ?Ⅳpatients with non?small cell lung cancer ( NSCLC) . Methods One hundred and twenty cases on stageⅢ?Ⅳpatients with NSCLC were randomly divided into two groups,60 cases received BJO combined with 125I and chemotherapy treatment(observation group),the other 60 cases received 125I combined with chemotherapy treatment(control group). Results The objective response rate(ORR) and disease control rate (DCR) were 71. 7%,86. 7% of observation group and 66. 7%,85. 0% of control group,there were no significant difference(χ2=0. 352,0. 069;P>0. 05) . The improvement rate of KPS score in observation group was significantly superior to that in control group, the difference was significant (76. 7% vs. 55. 0%;χ2=6. 261,P<0. 05) . The incidence of myelosuppression and gastrointestinal adverse e?vents in observation group was significantly lower that in control group ( 68. 3% vs. 83. 3%,41. 7% vs. 61. 7%;χ2=3. 883,4. 805;P<0. 05) . Conclusion BJO combined with 125I and chemotherapy for treating on stageⅢ?Ⅳ patients with NSCLC can reduce the toxicity and side effects caused by chemotherapy,and significantly im?prove the clinical symptoms and quality of life of patients.
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Aim To explore the inhibitory effects of ophiopogonin-B (OP-B ) on cell adhesion,invasion and migration in non-small cell lung cancer (NSCLC) A549 cells in vitro and its possible mechanism.Meth-ods Cell adhesion assay and transwell chamber assay were used to detect the ability of cell adhesion,migra-tion and invasion.qRT-PCR was used to detect the mRNA levels of MMP-2 and 9 .Meanwhile ,Western blot assay was performed to determine the protein levels of MMP-2/9 and p-Akt.Results OP-B significantly inhibited the ability of cell adhesion,invasion and mi-gration in A549 cells at the concentration of 10 μmol· L-1 (P<0.01 ).Meanwhile,it inhibited the mRNA and protein levels of MMP-2 and MMP-9 and down-regulated the phosphorylation of Akt (P <0.0 1 ). Conclusion OP-B inhibits cell adhesion,invasion and migration in A549 cells through down-regulation of the mRNA and protein expression of MMP-2/9 ,and the inhibitory effect on the expression of p-Akt.
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Aim To explore the effects of the inhibition of cell adhesion , invasion and migration in non-small cell lung cancer ( NSCLC ) H460 and A549 cells in-duced by platycodin-D ( PD ) and its mechanism. Methods Cell adhesion assay, wound-healing assay and Transwell chamber migration assay were used to detect the ability of cell adhesion, migration and inva-sion. Regulation of MMP-2 and MMP-9 mRNA was de-termined by RT-PCR. Meanwhile, Western blot was performed to determine the expression levels of MMP-2/9 , its upstream related proteins of ERK signaling pathway and p-Akt. Results PD effectively inhibited the ability of cell adhesion, invasion and migration in H460 and A549 cells in a dose-dependent manner ( P<0. 05 ) . PD reduced the expression of MMP-2 and MMP-9 mRNA in H460 and A549 cells ( P<0. 01 );meanwhile, PD down-regulated the expression levels of MMP-2/9 , and inhibited the expression of its upstream proteins Ras, p-c-Raf, p-ERK 1/2 and p-Akt in a time- and dose-dependent manner. Conclusions PD inhibits cell adhesion, invasion and migration in NSCLC cells, and these effects are related to the down-regulation of the expression of MMP-2 and MMP-9 mR-NA and protein, and inhibition of its upstream expres-sion of ERK signaling pathway and p-Akt.