2003
DOI: 10.1038/sj.onc.1206891
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Bcl-2 and Bcl-xL differentially protect human prostate cancer cells from induction of apoptosis by melanoma differentiation associated gene-7, mda-7/IL-24

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Cited by 123 publications
(160 citation statements)
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“…25 The P69 cells are normal human prostate epithelial cells immortalized by the SV40 T/t antigen and are cultured as described previously. 25 Cell viability was determined by standard MTT (3-(4, 5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide) assays.…”
Section: Methodsmentioning
confidence: 99%
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“…25 The P69 cells are normal human prostate epithelial cells immortalized by the SV40 T/t antigen and are cultured as described previously. 25 Cell viability was determined by standard MTT (3-(4, 5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide) assays.…”
Section: Methodsmentioning
confidence: 99%
“…25 The P69 cells are normal human prostate epithelial cells immortalized by the SV40 T/t antigen and are cultured as described previously. 25 Cell viability was determined by standard MTT (3-(4, 5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide) assays. 25 Construction of Ad.5/3-mda-7 The genome of Ad.5/3-mda-7 ( Figure 1a) was generated by homologous DNA recombination in Escherichia coli between linearized plasmid pShCMV.mda-7 and BstBIdigested genomic DNA of Ad.5/3-Luc1 vector.…”
Section: Methodsmentioning
confidence: 99%
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“…Each group was comprised of eight animals and the tumor growth was monitored and measured weekly and tumor volume (V) was calculated using the formula V (mm 3 ) ¼ length  width 2 /2. When the tumors were 100-150 mm 3 in size, mice were randomized into five groups and a daily dose of 5  10 8 PFU of examined viruses suspended in 100 ml of PBS or 100 ml PBS alone was administrated intratumorally for 4 days. At the end of the experiments, the tumors were harvested for histopathological and TdTmediated dUTP-biotin nick end labeling (TUNEL) analysis.…”
Section: Studies On Xenograft Tumors In Nude Micementioning
confidence: 99%
“…Earlier studies showed that expression of IL-24 by plasmid or replication-defective adenovirus that harbored IL-24 suppressed cell growth and induced apoptosis in a wide variety of cancer cell lines, including melanoma, breast, lung, cervix, colon and prostate carcinomas, but not normal cells. [2][3][4][5] However, the mechanism by which IL-24 induces its selective apoptosis is complicated, depending on the cell type studied. Previous studies have demonstrated that IL-24 can induce apoptosis at multiple levels by activating caspase cascade and upregulating P53, Bax, tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) and growth arrest and DNA damage protein family genes.…”
Section: Introductionmentioning
confidence: 99%