Therapeutic strategies for destroying cancer cells by making its death programs run again. The normal cell passes through several stages (Accumulation stage, Detoxification stage, Formation of free radical stage and A...Therapeutic strategies for destroying cancer cells by making its death programs run again. The normal cell passes through several stages (Accumulation stage, Detoxification stage, Formation of free radical stage and Activation of nuclear factor kappa B stage and the shutting down of programs of cell death stage) to become a cancerous cell. The success of the therapeutic strategy to treat cancer depends on making either one or both programs of cell death run again. Shutting down one stage completely will be sufficient to stop the transformation of the natural cell into a cancerous cell, which eliminates the production of hydrogen peroxide, thus the activity of the NF-Kb will be inhibited. However, shutting down all stages is the most comprehensive therapeutic strategy and guarantees treatment success.展开更多
Cancer is cell fleeing from death by blocking the intrinsic and extrinsic pathways of cell death programs. In the present work, the experimental formula was designed to remove these blockers. It was applied on 120 Swi...Cancer is cell fleeing from death by blocking the intrinsic and extrinsic pathways of cell death programs. In the present work, the experimental formula was designed to remove these blockers. It was applied on 120 Swiss albino mice which were inoculated intraperitoneally and subcutaneously with Ehrlich Ascites Carcinoma cells;1 × (106) cell/mouse. The activity of the cell death programs of the tumor was detected by measuring the volume of Ascites fluid, counting the number of dead cancer cells, measuring the size of the tumor, detecting the positive reaction of caspase enzyme in cancer cells and presence of macrophages and apoptotic bodies in tumor tissue. The experimental formula succeeded in removing the blockers of the cell death program in cancer cells returning the cell death program to work again.展开更多
OBJECTIVE: To examine whether a combinative treatment with curcumin enhances the effects of the epidermal growth factor receptor-tyrosine kinase inhibitor(EGFR-TKI) gefitinib on cell proliferation, clonogenic capacity...OBJECTIVE: To examine whether a combinative treatment with curcumin enhances the effects of the epidermal growth factor receptor-tyrosine kinase inhibitor(EGFR-TKI) gefitinib on cell proliferation, clonogenic capacity and apoptosis in the drug-resistant lung cancer cell line NCI-H1975, and further investigate the molecular mechanisms involved.METHODS: NCI-H1975 cells were treated with curcumin and gefitinib alone or in combination, and cell proliferation, clonogenic capacity and apoptosis were examined using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide(MTT) assay, clone forming experiments, and flow cytometry, respectively, while p38, extracellular regulated protein kinase(ERK)1/2, and protein kinase B(AKT)phosphorylation were examined using Western blotting.RESULTS: Compared with the effects of either agent alone, the combination of curcumin and gefitinib had a stronger suppressive effect on proliferation and the clonogenic capacity(P < 0.05), and showed an increased ability to promote apoptosis(P < 0.05) and reduce p38, ERK1/2, and AKT phosphorylation(P < 0.05).CONCLUSION: Co-treatment of curcumin and gefitinib significantly improves the ability of gefitinib to inhibit cell proliferation, suppress the clonogenic capacity and enhance apoptosis in NCI-H1975 cells,and these effects are possibly mediated via a decrease in phosphorylation of proteins in downstream pathways of the epidermal growth factor receptor.展开更多
文摘Therapeutic strategies for destroying cancer cells by making its death programs run again. The normal cell passes through several stages (Accumulation stage, Detoxification stage, Formation of free radical stage and Activation of nuclear factor kappa B stage and the shutting down of programs of cell death stage) to become a cancerous cell. The success of the therapeutic strategy to treat cancer depends on making either one or both programs of cell death run again. Shutting down one stage completely will be sufficient to stop the transformation of the natural cell into a cancerous cell, which eliminates the production of hydrogen peroxide, thus the activity of the NF-Kb will be inhibited. However, shutting down all stages is the most comprehensive therapeutic strategy and guarantees treatment success.
文摘Cancer is cell fleeing from death by blocking the intrinsic and extrinsic pathways of cell death programs. In the present work, the experimental formula was designed to remove these blockers. It was applied on 120 Swiss albino mice which were inoculated intraperitoneally and subcutaneously with Ehrlich Ascites Carcinoma cells;1 × (106) cell/mouse. The activity of the cell death programs of the tumor was detected by measuring the volume of Ascites fluid, counting the number of dead cancer cells, measuring the size of the tumor, detecting the positive reaction of caspase enzyme in cancer cells and presence of macrophages and apoptotic bodies in tumor tissue. The experimental formula succeeded in removing the blockers of the cell death program in cancer cells returning the cell death program to work again.
基金Supported by Natural Science Found of Zhejiang Province:Research of Molecular Mechanism of Curcumin Reversing TKI Targeted Drug Resistance of NSCLC(No.LY13H160037)
文摘OBJECTIVE: To examine whether a combinative treatment with curcumin enhances the effects of the epidermal growth factor receptor-tyrosine kinase inhibitor(EGFR-TKI) gefitinib on cell proliferation, clonogenic capacity and apoptosis in the drug-resistant lung cancer cell line NCI-H1975, and further investigate the molecular mechanisms involved.METHODS: NCI-H1975 cells were treated with curcumin and gefitinib alone or in combination, and cell proliferation, clonogenic capacity and apoptosis were examined using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide(MTT) assay, clone forming experiments, and flow cytometry, respectively, while p38, extracellular regulated protein kinase(ERK)1/2, and protein kinase B(AKT)phosphorylation were examined using Western blotting.RESULTS: Compared with the effects of either agent alone, the combination of curcumin and gefitinib had a stronger suppressive effect on proliferation and the clonogenic capacity(P < 0.05), and showed an increased ability to promote apoptosis(P < 0.05) and reduce p38, ERK1/2, and AKT phosphorylation(P < 0.05).CONCLUSION: Co-treatment of curcumin and gefitinib significantly improves the ability of gefitinib to inhibit cell proliferation, suppress the clonogenic capacity and enhance apoptosis in NCI-H1975 cells,and these effects are possibly mediated via a decrease in phosphorylation of proteins in downstream pathways of the epidermal growth factor receptor.
