2. COX expression in two bladder cancer cell lines, T24 and 5637, was examined after cells were stimulated with recombinant human epidermal growth factor (rhEGF) alone and combined with selective COX-2 inhibitor SC-58125 or nuclear transcription factor kappaB (NF-κB) inhibitor PDTC.
Conclusion 8-Br-cAMP could inhibited the expression of c-erbB-2,c-myc and mRNA in bladder carcinoma cells, it indicated that 8-Br-cAMP was an effective inhibitor for mitotic and proliferation of tumor cells.
Methods Hunman bladder carcinoma cell line T-24 was transfected with adenovirus expression vector containing TK gene and green fluorescent protein (GFP) gene, and the transfection efficiency was observed and TK expression detected by PCR.
Conclusion: The constructed chimeric antibody was expressed successfully in eukaryotic cells, and the chimeric antibody had desired affinity against human bladder cancer cells.
Effect of photodynamic therapy with BPD-MA on the proliferation and apoptosis of human bladder cancer cells
OBJECTIVE This study was conducted to explore the effect of Rg3 on inhibition of proliferation and induction of apoptosis in bladder cancer cells.
On Day 21 the tumors were resected and examined pathologically to see the immune response.Results: The observation of morphology of MBT-2 cells in vitro and MTT assay indicated that Allicin has apparent direct cytotoxicity to bladder cancer cells.
To study the effects of arsenic trioxide (As2O3) on the in vitro growth of human bladder cancer cells and the mechanisms.
The in vitro growth of bladder carcinoma cells was analyzed by MTT colorimetry, and the apoptosis rate was assayed by TUNEL methods.
Using this in situ assay method, we detected the reduced permeability to HRP in aortic and brain microvascular endothelial cells after 4-5 days culture with conditioned media of human astrocytes or bladder carcinoma cells.
In line with these data, expression of either p63RhoGEF or GEFT in J82 human bladder carcinoma cells induced the formation of actin stress fibres.
Nucleic acid metabolism of bladder carcinoma cells in vitro
Nucleic acid metabolism was investigated to determine the metabolic activity of bladder carcinoma cells.
Expression of a mutant hTERT in human bladder carcinoma cell line T24 and its clinical significance
After transfecting the fusion gene into bladder carcinoma cell line T24 by calcium phosphate-DNA coprecipitation, the steady expression of GFP-hTERT fusion protein was tested by fluorescent light microscopy.
The proliferation changes of bladder carcinoma cell line T24 were detected by light microscopy and senescence correlated β-galactosidase staining.
Conclusion: The mutant-type hTERT gene suppresses the proliferation of bladder carcinoma cell line T24 by competitive effect on telomerase activity.
Apoptosis induced by ginsenoside Rg3 in a human bladder carcinoma cell line