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1.
AIM: To study the effect and mechanism of yeast cytosine deaminase/ thymidine kinase (yCD/TK) double suicide gene driven by alpha fetoprotein (AFP) promoter on hepatocellular carcinoma (HCC) in vitro and in vivo. METHODS: The expression plasmid with yCD/TK double suicide gene, which was driven by AFP promoter, was constructed. HepG2 (AFP positive) and SMMC7721 (AFP negative) human HCC cell lines were both transfected with the above-mentioned expression plasmid through cationic liposome. The cells were treated with 5-fluorocytosine (5-FC) and/or ganciclovir (GCV) at different concentrations. The cell proliferation and cell cycle phase were evaluated by MTT test and flow cytometry respectively. The effect of double suicide gene on HCC xenografts in nude mice was observed through measuring the tumor size and the number of apoptosis cells. RESULTS: The double suicide gene was expressed selectively on HepG2 cells, rather than on SMMC7721 cells. The 5-FC and/or GCV inhibited effectively the proliferation of HepG2 cells in a dose-dependent manner, but had no influence on SMMC7721 cells. The inhibitory effect on HepG2 cells among different treatments was GCV+5-FC>5-FC>GCV. In vivo, the treatments inhibited markedly the growth of HepG2 cell xenografts in nude mice, transfected with yCD/TK gene. More apoptotic cells were found in HepG2 xenografts after the treatment. However, the growth of SMMC7721 cell xenografts could not be inhibited by this double suicide gene therapy, and few apoptotic cells were found. CONCLUSION: yCD/TK double suicide gene driven by AFP promoter has a significant efficacy in treatment of AFP positive HCC. Cell apoptosis may be an important mechanism of yCD/TK double suicide gene-inhibiting the growth of HCC.  相似文献   

2.
Cytosine deaminase (CD) gene is a kind of suicide gene, cytosine deaminase can catalyze the conversion from 5-fluorocytosine (5-FC) into 5-fluorouracil (5-FU), this combination therapy (CDgene/5-FC) were widely used in cancer therapy. The results of many researches in different cancer cells have demonstrated that it can inhibit tumor growth significantly. The mechanism includes 5-FU’s direct killing tumor cells and its bystander effect. It can also be used as a potential purging method for autologous hematopoietic cells transplantion after chemotherapy in breast cancer patients. CD/5-FC combined with other therapies would be an important future research approach.  相似文献   

3.
AIM: To facilitate the suicide gene delivery into neoplasm, a chimeric gene of HSV-tk and green fluorescent protein (gfp) was constructed. METHODS: Molecular cloning technique was used to construct this kind of eukaryotic vector. The internal ribosome entry site (IRES) of encephalomyocarditis virus (EMCV), which could coordinate expression of two genes in a single vector, was optioned. By using liposome-mediated transfection, eukaryotic expression vector tgCMV/hytk-IRES-gfp was transfected into human bladder carcinoma cells EJ. RESULTS: A bicistronic eukaryotic vector carrying gfp and hygromycin phosphotransferase-thymidine kinase fusion (hytk) gene was constructed. The results of PCR and microscopy detection show that the hytk-IRES-gfp gene was successfully transferred into EJ cells. There were no differences in the growth pattern or the morphology between EJ and EJ/hytk-GFP cells. In vitro experiments demonstrated dose- and time-dependent cell killing by transduction of the hytk-IRES-gfp gene followed by GCV treatment. The IC50 (the concentration required to elicit 50% growth inhibition) was 2.16 mg/L in treatment with GCV for 72 hours. CONCLUSION: These results suggest that this new kind of eukaryotic vector could serves as a new tool and method for neoplasm gene therapy.  相似文献   

4.
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5.
AIM:To elucidate the pattern of 5-fluorocytosine(5-FC) induced apoptosis and its role in gene therapy for human pancreatic cancer. METHODS: The human pancreatic cancer SW1990 cells(CEA-producing) were infected with recombinant adenoviruses(Adex1CEA-prCD or Adex1CEA-prZ).Cytosine deaminase(CD) expression was examind by western blot. Apoptosis induced by 5-FC in human pancreatic cancer SW1990 cells genetically modified to express cytosine deaminase was investigated by applying electron microscopy, DNA electrophoresis and flow cytometry analysis techniques. RESULTS: The SW1990 cells infected with Adex1CEA-prCD were treated with 5-FC at 100 μmol·L-1 for 48 h, cell apoptosis occurred. Typical apoptosis morphological feature appeared and DNA ladder could be demonstrated on DNA electrophoresis. Apoptosis peak was also showed by flow cytometry. Apoptotic cells accounted for 34.6% of the cell population. Cells in G1, S and G2/M phase of cell cycle were 64%, 11% and 7%, respectively. CONCLUSION: The apoptosis induced by 5-FC may be a primary mechanism in CD gene therapy for pancreatic cancer.  相似文献   

6.
AIM:To construct the shuttle plasmid vector for thymidine kinase(tk) and EGFP fusion protein gene driven by IGF-Ⅱ P3 promoter,and investigate the specific killing effect of the HSV-tk/GCV system on hepatocellular carcinoma(HCC) cells in vitro.METHODS:Recombinant shuttle plasmid vector was constructed by techniques of genetic recombination and screening,and identified by restriction digestion and sequencing analysis. Then the recombinant shuttle plasmid was transfected into HepG2 and HeLa cells by techniques of lipofectamine transfection and its expression was detected by fluorescence microscope and RT-PCR. Cell killing after ganciclovir(GCV) application was determined by MTT.RESULTS:Identification of pDC316-tkEGFP-P3 by enzyme digestion and sequencing analysis showed that the length,inserted location and direction of the target genes which were inserted into the recombinant were correct. It was found that enhanced green fluorescence protein could only be seen in HepG2 cells,but not in HeLa cells. The results of RT-PCR showed that only two bands could be seen in the samples of pDC316-tkEGFP-P3 transfected HepG2 cells. The MTT test showed the selective cytotoxicity of GCV to the transfected HepG2 cells.CONCLUSION:The shuttle plasmid vector carrying the tkEGFP fusion protein gene driven by IGF-Ⅱ P3 promoter has been constructed successfully and its specific expression in HepG2 cells provided a sound basis for targeted gene therapy for HCC.  相似文献   

7.
AIM:To observe the chemosensitization effect of methylseleninic acid (MSA) on human triple-negative breast cancer (TNBC) cells. METHODS:MDA-MB-231 cell line was co-cultured with MSA plus paclitaxel or doxorubicin. The inhibitory rate of cell proliferation was detected by CCK-8 assay. The combination index was calculated to explore the impact of MSA on the efficacy of chemotherapeutic drugs. The cell cycle was analyzed by flow cytometry. Annexin V-FITC/PI double staining was applied to detect the cell apoptosis. RESULTS:Compared with single usage of chemotherapeutic drugs, the cell proliferation rates were decreased when the chemotherapeutic drugs was combined with MSA, suggesting that there is a synergistic relationship between MSA and chemotherapeutic drugs. Compared with the single-agent groups, the G2/M-phase cells in paclitaxel combined with MSA group increased significantly (P<005),and the S-phase cells increased significantly in doxorubicin combined with MSA group (P<005). These suggested that MSA enhanced the anticancer effect of the drugs by inducing cell cycle arrest. Compared with single usage of 10 nmol/L paclitaxel, the apoptotic rate increased from 41.1% to 59.3% (P<005) as 10 nmol/L paclitaxel combined with 3.5 μmol/L MSA was used. Compared with single usage of 0.5 μmol/L doxorubicin, the apoptotic rate increased from 30.2% to 51.9% (P<0.01) as 0.5 μmol/L doxorubicin combined with 3.5 μmol/L MSA was used. These suggested that MSA enhanced antitumor effect of the drugs by inducing tumor cell apoptosis. CONCLUSION: MSA enhances the antitumor effects of chemotherapeutic drugs doxorubicin and paclitaxel on TNBC cells. One of the possible mechanisms is the enhancement of inducing tumor cell apoptosis and cell cycle arrest.  相似文献   

8.
AIM: To explore the effects of mammalian target of rapamycin (mTOR) double inhibitor AZD8055 on autophagy and apoptosis of human cholangiocarcinoma cell line HuCCT1. METHODS: The effect of AZD8055 on the viability of HuCCT1 cells was detected by MTT assay. Autophagosome was detected by acridine orange (AO) staining. After treated with AZD8055, the expression levels of apoptosis-related proteins Bcl-2, Bax and cleaved caspase-3 and auto-phagy marker proteins beclin 1, LC3 and p62 were determined by Western blot. Apoptotic rate was analyzed by flow cyto-metry with Annexin V-FITC/PI double staining. RESULTS: AZD8055 significantly inhibited the viability of HuCCT1 cells (P<0.05). AO staining showed that AZD8055 significantly increased orange granules in the cytoplasm. After treated with AZD8055, compared with the control group, the protein level of beclin 1 and the ratio of LC3-Ⅱ/LC3-I were enhanced, while p62 was attenuated (P<0.05). The protein expression level of pro-apoptotic regulator Bax was down-regulated and anti-apoptotic regulator Bcl-2 was increased. The protein level of cleaved caspase-3 was reduced (P<0.05). The results of flow cytometry showed that AZD8055 inhibited cell apoptosis. CONCLUSION: AZD8055 inhibits the viability of cholangiocarcinoma cells, and the mechanism is closely related with autophagy induced by AZD8055.  相似文献   

9.
AIM: To investigate the in vitro antitumor immune responses of dendritoma formed by mouse hepatocellular carcinoma cells and lymphotactin gene modified dendritic cells (DCs). METHODS: DCs prepared from mouse bone marrow were genetically modified by lymphotactin adenovirus, and fused with H22 cells by polyethylene glycol. RT-PCR and ELISA were employed to identify lymphotactin expression at mRNA and protein levels. The phenotypes and fusion efficiency were detected by FACS. The stimulatory capacity of DC to T cells was detected by mixed leukocyte reaction. The cytotoxicity activity against H22 cells was assayed by LDH method. RESULTS: Lymphotactin effectively expressed by DCLptn/H22 hybridoma. DCLptn/H22 cells induced potent T cell proliferation effect and generated strong CTL reaction against allogenic H22 cells. CONCLUSION: Lymphotactin genetic modification enhanced the in vitro immune activity of dendritoma.  相似文献   

10.
AIM: To study the inhibitory effect of VEGF-C/Flt-4 system on lymphangiogenesis and lymphatic metastasis of breast cancer. METHODS: Lymphatic endothelial cells (LEC) were cultured in vitro, the effects of VEGF-C and anti-Flt-4 antibody on the proliferation of treated cells were observed. The antisense oligodeoxynucleotides (ASODN) targeting VEGF-C was designed and its effect on VEGF-C gene expression in vitro experiments was observed. The nude mice transplantation tumor model was made and the effects of VEGF-C ASODN on lymphangiogenesis and metastasis in the model were determined. RESULTS: The supernatant of cultured PC3 cells promoted LEC proliferation obviously while the cells treated with anti-Flt-4 antibody were obviously decreased whenever cell counting. The mRNA and protein expression of VEGF-C in MCF-7 cells treated with ASODN were significantly lower than that in control groups in vitro. In vivo ASODN also significantly reduced the VEGF-C mRNA expression detected by RT-PCR. The result of 5-Nase-ALPase enzyme -histochemistry showed that ASODN had obvious inhibitory effect on tumor lymphangiogenesis. Tumor growth velocity in ASODN group was much slower than that in control group. ASODN also inhibited tumor volume and lymphatic metastasis. CONCLUSION: The strong relationships between VEGF-C/Flt-4 system and lymphangiogenesis and lymphatic metastasis of breast cancer have been observed. If the expression of Flt-4 is blocked, the proliferation of LEC induced by tumor cells can be blocked in some degree. ASODN inhibits tumor lymphangiogenesis and lymphatic metastasis by down-regulating VEGF-C expressions.  相似文献   

11.
AIM: To study the effect of monocyte/macrophages treated with CpG-oligodeoxynucleotides on leukemic K562 cells. METHODS: The monocytes/macrophages from peripheral blood cells were isolated and induced. The expressions of CD14 and CD16 on monocytes/macrophages were detected by means of flow cytometry. After treated with synthetic CpG-oligodeoxynucleotides, and nonCpG-oligodeoxynucleotides for 24 hours respectively, the inhibiting effect of monocyte/macrophages on K562 cells were detected using MTT method. The secretions of TNF-α and IL-12 from monocytes/macrophages were determined using ELISA method. RESULTS: The monocytes/macrophages treated with CpG-oligodeoxynucleotides enhanced their antitumor effect on K562 cells and increased the secretion levels of TNF-α and IL-12. Whereas, there was no significant difference between antitumor effect and cytokine secretion of the monocytes/macrophages treated with nonCpG-oligodeoxynucleotide. CONCLUSION: CpG-oligodeoxynucleotides increases the cytotoxicity of macrophages on K562 cells in vitro, as well as facilitates the IL-12 and TNF-α secretion. It provides a new approach for immunologic treatment of leukemia.  相似文献   

12.
AIM：To explore the effect of SET and MYND domain-containing protein 3 (SMYD3) over-expression on miR-124 expression and proliferation ability of human intrahepatic cholangiocarcinoma cells. METHODS：Transient transfection of SMYD3 eukaryotic expression plasmid into human intrahepatic cholangiocarcinoma cell line HCCC-9810 were performed. The expression of SMYD3 at mRNA and protein levels was measured by qRT-PCR and Western blotting, respectively. The expression of miR-124 was detected by qRT-PCR, and the methylation status of miR-124 gene was determined by methylation-specific PCR. Cell proliferation was examined by CCK-8 assay and colony formation experiment. RESULTS：After transfected with SMYD3 eukaryotic expression plasmid, the over-expression of SMYD3 in HCCC-9810 cells was observed. Compared with the blank cells, the expression level of miR-124 was significantly decreased and miR-124 gene promoter methylation was significantly increased. In addition, SMYD3 over-expression significantly promoted the proliferation of HCCC-9810 cells. CONCLUSION：The transient transfection of SMYD3 plasmid increases the methylation of miR-124 gene promoter and induces under-expression of miR-124. Over-expression of SMYD3 promotes the proliferation of cholangiocarcinoma cells.  相似文献   

13.
AIM: To investigate the antitumor effects of tumor necrosis factor-α (TNF-α) and interferon-γ (IFN-γ) on hepatocellular carcinoma (HCC). METHODS: Cytotoxicity of the combination of TNF-α and IFN-γ on HCC in vitro was measured by using a crystal violet (CV) staining method. Antitumor effects of the combination of TNF-α and IFN-γ on HCC in vivo were observed by intra-hepatic injection of TNF-α and IFN-γ to the tumor in a human HCC nude mice hepatic model. RESULTS: The growth of HCC cells was inhibited by TNF-α alone, which was dose-dependent. The cytotoxicity of TNF-α on HCC was enhanced by incubation with IFN-γ. TNF at 107 U/L, or IFN-γ at 106 U/L alone killed only 27.1% or 7.9 of HCC cells, respectively, when combined with IFN-γ, it killed 83.7% of HCC cells. A synergistic antitumor effect on HCC in vivo was observed in combination group, as tumor growth inhibition rate was 35.9% compared with 17.2% in TNF-α group and 5.6% in IFN-γ group. The survival period of mice bearing tumor was significantly prolonged and serum AFP was significantly decreased in combination group (P<0.05). Tumor necrosis was observed to be much severer in combination group. CONCLUSION: Our results suggest that the combination of TNF-α and IFN-γ by intratumor injection is a promising adjunctive modality to treat HCC.  相似文献   

14.
DING Guo-fu  LI Bin  WU Chong  LUO Ping  LI Jun  ZHOU Hong 《园艺学报》2008,24(10):2025-2028
AIM: To investigate whether alteration of the core sequence of CpG ODN change its cellular interanalization and immunological activity. METHODS: 6-FAM labeled CpG ODN was artificial synthesized and the CpG dinucleotide was altered by cytosine methylation (mCpG ODN) and/or CG sequence reversal (GpC ODN). RAW264.7 cells were cultured in vitro. After stimulated with different 6-FAM labeled ODN, the accumulation of ODN in the cells were measured by flow cytometry. RAW264.7 cells grown on glass coverslips were pretreated with each ODN and subsequently the localization of ODN in cells were observed by confocal scanning microscopy. Meanwhile, the level of TNF-α in supernatant was tested by ELISA. RESULTS: The alteration of the core sequence of CpG ODN didnt influence its accumulation in RAW264.7 cells. In vitro, 6-FAM labeled ODN was internalized into RAW264.7 cells and a few green fluorescent dots were widely distributed over cytoplasm. Large amount of TNF-α were released from RAW264.7 cells stimulated by CpG ODN. However, after methylation of cytosine in CpG dinucleotide, the TNF-α release was significantly decreased (P<0.01). At the same time, CG sequence reversal of CpG dinucleotide completely abolished the stimulated activity of CpG ODN. CONCLUSION: Its essential for the biological function of CpG ODN with certain CG sequence. The methylation of cytosine in CpG dinucleotide doesnt influence the internalization and localization of CpG ODN in RAW264.7 cells, but partially inhibit its immunological activity.  相似文献   

15.
AIM: To observe the antitumor effect of 5 commonly used chemotherapeutic drugs on 11 human colorectal cancer cell lines in vitro. METHODS: CCK-8 method was used to determine the growth inhibitory effects of 5 antitumor drugs, which were expressed as the half growth inhibitory concentration (IC50) and sensitivity index IC50/PPC (peak plasma concentration) on 11 human colorectal cancer cell lines. The expression variations of heat-shock protein 27 (HSP27) and HSP70 at protein levels in human colorectal tumor cell lines treated with different chemotherapeutic drugs were observed by Western blotting. RESULTS: All the 11 colorectal cancer cell lines were sensitive to 5-fluorouracil (5-FU) and oxaliplatin (OHP) without drug resistant. Five colorectal cancer cell lines were sensitive to mitomycin (MMC), while the other 6 cell lines were moderately sensitive. Ten colorectal cancer cell lines except SW1116 were sensitive to docetaxel (DXL), while SW1116 cells were resistant to DXL. Nine colorectal cancer cell lines except LS174T and SW1116 were moderately sensitive to irinotecan (IFL), and SW1116 cells were also resistant to IFL, while LS174T cells were sensitive to IFL. After treated with the antitumor drugs, HSP27 was up-regulated in HCT116 cells and SW480 cells, while the expression of HSP70 didnt change. CONCLUSION: LS174T cells are multidrug-sensitive, while SW1116 cells are multidrug-resistant. 5-FU and OHP are the wide-spectrum anti-colorectal cancer drugs. Determining the sensitivity to chemotherapeutic drugs and the expression level of HSP27 can improve the accuracy in drug selection.  相似文献   

16.
AIM: Plasmid Egr-IL18-B7.1 was constructed to explore its expression characteristics induced by different doses of radiation and its suppressive effect on melanoma under radiotherapy. METHODS: The plasmid containing both IL-18 and B7.1 genes downstream of Egr-1 was constructed using gene recombination technique. The in vitro expression of IL-18 and B7.1 induced by ionizing radiation was measured with ELISA and flow cytometry, respectively. The effect of gene radiotherapy on malignant melanoma was assayed by observing the growth rate of B16 cells implanted into C57BL/6J mice. RESULTS: Effective expression of IL-18 and B7.1 by plasmid Egr-IL18-B7.1 treated with different doses of X-irradiation were observed and in vivo experiments showed significant inhibition of tumor growth after combined gene-radiotherapy. CONCLUSION: Data presented in this paper implicate that gene radiotherapy with plasmid containing double genes might be one of the effective anticancer therapeutic measures.  相似文献   

17.
AIM: To evaluate the antitumor effect of caffeic acid Ge on U14 tumor bearing mice. METHODS: The tumor inhibitory ratios of caffeic acid Ge on the growth of U14 in mice was observed. Apoptosis morphological transformation of U14 cells induced by caffeic acid Ge was detected by electronic scan microscope and MG-P staining. Alteration of cell cycle was analyzed by flow cytometry. Apoptosis-related protein levels of Bax and Bcl-2 were determined by immunity histochemistry technology. MTT assay was applied to study the antitumor activities of caffeic acid Ge in U14 cell lines in vitro. RESULTS: Tumor inhibitory rates in caffeic-acid Ge groups were 38.50%, 47.17% and 64.02% (from low dose to high dose) (P<0.01). Caffeic acid Ge induced apoptosis in U14 cells detected by MG-P staining, histopathology and electronic microscopy, the typical apoptosis characteristics in morphology were observed. Flow cytometry results indicated that most of the U14 cells treated with caffeic acid Ge were arrested at the sub-G0-G1 phase and the U14 cells were blocked in S phase. The results of immunity histochemistry indicated that the expression of Bcl-2 protein was down-regulated by caffeic acid Ge while Bax protein was up-regulated in U14 tumor tissue (P<0.05). The MTT results suggested that cafffeic acid Ge exhibited high antiproliferative activity in U14 cell lines, and the IC50 for 48 h was 48.57 mg/L. The above results showed that caffeic acid Ge exhibited high antiproliferative activity in vitro. CONCLUSION: Caffeic acid Ge has antiproliferative and proapoptotic effect on U14 tumor cells in vivo and in vitro. Caffeic acid Ge increases the expression of Bax and decreases the expression of Bcl-2 to induce apoptosis of U14 cells. This is one of the possible mechanisms of antitumor.  相似文献   

18.
Abstract: AIM: To investigate the effects of esophageal cancer-related gene 2 (ECRG2) protein combined with cisplatin (DDP) on the proliferation and apoptosis of human esophageal cancer EC9706 cells. METHODS: Methylthiazolyl tetrazolium (MTT) assay was used to examine the effects of single ECRG2 protein and ECRG2 protein combined with DDP on the proliferation of EC9706 cells. Hoechest 33258 staining was applied to analyze the effect of single ECRG2 protein and ECRG2 protein combined with DDP on apoptosis of EC9706 cells. The expression of p53 in EC9706 cells was detected by Western blotting. RESULTS: ECRG2 protein inhibited the proliferation of EC9706 cells. ECRG2 protein combined with DDP enhanced the inhibitory effect time- and dose-dependently in a certain range of concentrations. The number of apoptotic cells after treated with ECRG2 protein combined with DDP for 24 h was larger than those treated with single ECRG2 protein. The proliferation-inhibitory and qpoptosis-inducing expression of p53 was up-regulated in ECRG2 protein and DDP combination group compared with single ECRG2 protein group. CONCLUSION: DDP enhances the proliferation-inhibitory and apoptosis-inducing effects of ECRG2 protein on EC9706 cells. The apoptosis-inducing mechanism may be related to the up-regulation of p53 expression.  相似文献   

19.
ZHENG Ying  JIANG Kai 《园艺学报》2015,31(9):1578-1583
AIM: To determine whether imperatorin would enhance the effect of doxorubicin therapy on cervical cancer in vitro.METHODS: The viability of HeLa cells treated with imperatorin and doxorubicin was determined by MTT assay in vitro. The expression of Bcl-2 protein family(Mcl-1, Bcl-2, Bcl-xL, Bad and Bax) in HeLa cells treated with imperatorin and doxorubicin was evaluated by Western blot analysis. The apoptosis and mitochondrial membrane potential(ΔΨm) in the HeLa cells treated with imperatorin and doxorubicin were analyzed by flow cytometry. A Mcl-1 expression vector was constructed, and its role in the cytotoxicity of imperatorin plus doxorubicin to HeLa cells was detected by MTT assay.RESULTS: Addition of imperatorin significantly enhanced the cytotoxicity of doxorubicin to HeLa cells in vitro. Mcl-1 expression was down-regulated by imperatorin but was not influenced by doxorubicin in the HeLa cells. A combination of imperatorin and doxorubicin induced apoptosis and ΔΨm collapse more significantly compared with the treatment with imperatorin or doxorubicin alone. Furthermore, the imperatorin-induced sensitization for doxorubicin cytotoxicity to HeLa cells was abolished by the transfection with Mcl-1 expression plasmid.CONCLUSION: The combination of doxorubicin with imperatorin enhances the antitumor effect of doxorubicin on cervical cancer cells via targeting Mcl-1.  相似文献   

20.
AIM: ZD1839 and trastuzumab are reported to improve the therapeutic efficacy of treatment for non-smallcell lung cancer (NSCLC) and breast cancer, respectively, although the effectiveness of either drug alone is not satisfactory. NSCLC cells often express both EGFR and HER2. We therefore investigated whether a combination of ZD1839 and trastuzumab had an additive or synergistic antitumor effect. METHODS: MTT was used to measure the inhibitory effects of ZD1839 (iressa) and trastuzumab (herceptin) on the growth of A549 cells. The cell apoptosis was studied by DAPI staining, and Annexin V/PI double labeling. RESULTS: The inhibitory action of cell growth was seen in A549 cells dealing with ZD1839 and trastuzumab. They inhibited the growth of the human lung cancer cell line A549 in a concentration and time dependent manners. Compared with either ZD1839 or trastuzumab alone, combination with curcumin respectively increased the growth inhibition rate and increased apoptosis of A549 cells (P<0.05) significantly, suggesting the synergistic actions of the two drugs. CONCLUSION: The results suggest that combination treatment with ZD1839 and trastuzumab might have improved therapeutic efficacy against NSCLC cells expressing both EGFR and HER2.  相似文献   

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