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Objective: To investigate the effect of astragaloside IV on tumor cellular uptake and antitumor efficacy by ginsenoside compound K (GCK). Methods: The human lung adenocarcinoma cell line A549 was prepared as an antitumor model, the cytotoxicity of the mixtures of GCK and astragaloside IV to A549 cells was determined by MTT assay, the cellular uptake of GCK was detected by fluorescence microscopy, and the intracellular GCK was determined by HPLC. The enhancement of astragaloside IV in vivo efficacy by GCK was evaluated by nude mice bearing tumor model. Results: The effect of GCK on the inhibition of A549 cell proliferation was enhanced in the presence of astragaloside IV and astragaloside IV could increase the uptake rate of GCK in A549 cells, with the proportion of astragaloside IV increasing, the cytotoxicity was significantly stronger than GCK and the uptake rate was improved. In vivo antitumor assay of mice bearing tumor indicated that astragaloside IV could enhance the antitumor efficacy of GCK. Conclusion: Preliminary results indicate that the mixture of GCK and astragaloside IV have the effect of enhancing antitumor efficacy.
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Aim To investigate the cytotoxic effect and mechanism of ampelopsin sodium ( AMP-Na ) on hu-man lung adenocarcinoma cell line GLC-82 alone or combined with carboplatin ( CBP ) . Methods The cytotoxic effect of human lung adenocarcinoma cell line GLC-82 was investigated by 3-(4,5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide ( MTT ) colori-metric assay. Ultrastructure change of apoptotic GLC-82 cells was observed with transmission electron micro-scope. The changes of the cell apoptosis and the ex-pression of caspase-3 were analyzed with flow cytome-ter. Results Combined with AMP-Na, the IC50 of CBP decreased from (17. 10 ± 4. 78) mg·L-1 to tron microscope and flow cytometric analysis, the apop-tosis and necrosis ratios also increased in the combina-tion group. The necrosis ratios increased from (2. 56 ± 0. 41 )% to ( 71. 83 ± 5. 43 )% ( P<0. 01 ) . The ex-pression of caspase-3 was increased significantly after treated with AMP-Na or combined with CBP. Conclu-sions There is a synergistic cytotoxic effect on GLC-82 cells treated with AMP-Na combined with CBP. Ap-optotic cells and necrotic cells are found in GLC-82 cells treated with AMP-Na alone or combined with CBP. One of the mechanisms to induce apoptosis is probably that activation of caspase-3 mediates signal transduction pathway in cells.
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In order to investigate the inhibitory effects of Endostar(rh-endostatin,YH-16)in combination with radiotherapy on lung adenocarcinoma A549 in mice and the interaction mechanisms of combined therapy,the transplantation tumor models of A549 lung adcnocarcinoma were established.When the largest diameter of tumor reached 1.0 cm,all nude mice were randomly divided into 4 groups: Endostar group,radiotherapy group,radiotherapy plus Endostar(combined treatment)group,and control group(n=6 in each group).The largest diameter and the vertical diameter of tumor were measured at different time points.At the 16th day,mice were executed,and the tumors were applied to analysis of rate of tumor cell apoptosis,and the expression levels of basic fibroblast growth factor(bFGF)mRNA were detected by reverse transcription-polymerase chain reaction(RT-PCR)and those of vascular endothelial growth factor(VEGF)by immunohistochemistry.The results demonstrated that the rate of tumor inhibition in combined treatment group was higher than that in other groups.And the rate of tumor cell apoptosis in combined treatment group was also higher than that in other groups.Meanwhile,the levels of bFGF mRNA and VEGF expression in combined treatment group were lower than those in other groups.It was concluded that Endostar obviously enhanced the curative effectiveness of radiotherapy on lung adenocarcinoma A549 in mice.The underlying mechanisms may involve the down-regulation of bFGF mRNA and VEGF expression to inhibit angiogenesis by Endostar and the cooperative effect of Endostar and radiotherapy to synergistically promote tumor cell apoptosis.And Endostar inhibits angiogenesis by down-regulating the expression of bFGF mRNA and VEGF.
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Objective:To investigate the radiosensitization and the cell-cycle of mild hyperthermia(≤42℃)on human pulmonary adenocarcinoma cell line SPC-A-1 in vitro. Methods: The human pulmonary adenocarcinoma cell line SPC-A were treated with radiation and the combination of radiation with mild hyperthermia. Radiosensitivity was determined by clonogenic assay and quantified by calculating the thermal enhancement ratio (TER). Flow cytometry was used to observe the cell-cycle. Results: Do, Dq calculated from the dose-response curve for radiation combined with 41.5℃ were 1.390 Gy, 1.426 Gy, whereas 1.693 Gy, 2.453 Gy for radiation alone, respectively. TER was 1.218. The proportion of cells in S phase was found to be 14.81% in the radiation group. The values, after 48 hours and 72 hours, with 6Gy radiation combined immediate 41.5℃ one hour mild hyperthermia, were 5.89% and 9.08%, respectively, versus 18.8% and 31.91% with 6 Gy radiation alone. Conclusion:Radiosensitization of mild hyperthermia in SPC-A-1 cells associated with the hyper-radiosensitization of the cells in S phase.
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Objective To study the effect of the recombinant matrilysin (rMMP-7) and its antisense oligonucleotide transfected by liposome (LIPO-MAON) on the proliferation of lung adenocarcinoma cell line A549 and human umbilical vein endothelial cells (HUVEC). Methods Antisense oligonucleotide of matrilysin was constructed by liposome transfection. The proliferation of HUVEC and A549 was detected by MTT assay in case of rMMP-7 or LIPO-MAON existence. The expression of MMP-7 mRNA in both HUVEC and A549 was examined by semi-quantitative RT-PCR assay. Results The proliferation of both HUVEC and A549 cell line was accelerated by high level of rMMP-7 (0.75, 1.0 ?g/ml), and the inhibited proliferation was only found in A549 cell line treated with high concentration of LIPO-MAON (7.5, 10 nmol/ml), but not in HUVEC. By RT-PCR assay, no expression of MMP-7 mRNA was found in HUVEC; however, enhanced or decreased expression of mRNA were found when A549 cell line was treated respectively with rMMP-7 or LIPO-MAON (P
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Objective:To investigate the inhibitory effects of cytokine induced-killer(CIK) cells combined with docetaxel(DTX) on the expansion of lung adenocarcinoma cell line SPC-A1/DTX in vitro and in vivo.Methods:Peripheral blood mononuclear cells(PBMC) from healthy donors were incubated in vitro to induce CIK cells in the presence of interferon-gamma(IFN-?),IL-2 and anti-CD3 monoclonal antibody.MTT assay was employed to evaluate the cytotoxic activity of DTX,CIK cells and their combination against SPC-A1/DTX cells in vitro.SPC-A1/DTX lung adenocarcinoma cells were injected subcutaneously into nude mice.On the 14 th day,normal saline(control group),docetaxel(DTX 1 mg/kg in 0.2 ml,DTX group),CIK cells(1?107,CIK group),and CIK cells combined with docetaxel(CIK+DTX group) were administered intraperitoneally respectively.All the nude mice were sacrificed at day 15 after treatment and the tumor were weighted out.Results:MTT assay showed that the IC50 to docetaxel in SPC-A1/DTX cells was 110.5 ?g/ml and 8.5 ?g/ml in wild SPC-A1 cells.CIK cells possessed a higher anti-tumor cytotoxic activity in SPC-A1/DTX cells in vitro than in wild SPC-A1 cells(P
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Objective To observe the effects of arsenic trioxide(As2O3)on the expressions of TNF-?,Fas and bcl-2 in lung adenocarcinoma cells(LAC)and to explore the mechanism of arsenic trioxide inducing apoptosis.Methods The expressions of TNF-?,Fas and bcl-2 in lung adenocarcinoma cells pretreated by arsenious acid were determined by the double antibody sandwich ABC-ELISA method.Results Compared with the control group,As2O3 showed no effects on the contents of bcl-2 in lung adenocarcinoma cells after 72 hours treatment,but increased the contents of TNF-? and Fas significantly,and the effects in different concentration groups had significant differences.The protein expressions of TNF-? and Fas showed a tendency of concentration-dependent increasing.Conclusions The results suggest that As2O3 induces the apoptosis of LAC cells possibly by up-regulating the expression of TNF-? and Fas.
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Objective To investigate the possibility of inhibiting the malignant proliferation of tumor cells in vitro through down-regulating the expression of MMP-7 by antisense gene technology. Methods A Phosphorothioate antisense oligodeoxynucleotide (ASODN) and scrambled oligodeoxynucleotide (SCODN) against MMP-7 were respectively transfected into A549 cells mediated by liposome. The expression of MMP-7 and cell proliferation in the cells were respectively examined by immunohistochemical assay and MTT. Flow cytometry was used to detect the cell cycles. Results After A549 cells were transfected with MMP-7 ASODN, the cell number was decreased. MTT method indicated that the proliferation of A549 cells was inhibited by MMP-7 ASODN at different concentrations, with the inhibition reaching the peak at 48 h. ASODN transfection downregulated the expression levels of MMP-7 protein, and inhibited the transition period of G_ 0 /G_ 1 phase to S phase. Conclusion The artificial MMP-7 ASODN can specifically inhibit the expression of MMP-7 protein and regulate cell cycle and cell proliferation in A549 cells.