t24 human urinary bladder cancer cell line Search Results


t24 human urinary bladder cancer cells  (Coriell Institute for Medical Research)
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Coriell Institute for Medical Research t24 human urinary bladder cancer cells
( a ) <t>T24</t> bladder cancer cells, which harbor the c.35G>T mutation, were transfected with HRAS minigenes with either a wild type or an optimized 3’ splice site and treated either with an SSO (SSO-A) that blocks access to the ESE or a scrambled control SSO. SSO-A treatment mediates exon 2 skipping from the wild type HRAS minigene, but this is alleviated when optimizing the 3’ splice site. ( b ) SSO-A treatment causes nearly complete skipping of endogenous HRAS exon 2 in T24 cells. ( c ) Western blot analysis confirmed reduced levels of HRAS protein following SSO-A treatment. ( d ) Quantification of cell viability after SSO-A treatment by WST-1 assay demonstrates that it decreases viability of T24 bladder cancer cells. ( e ) xCelligence real time monitoring of proliferation of T24 bladder cancer cells. Cells were treated with either SSO-A or control SSO at two concentrations (20 nM or 30 nM). When treated with SSO-A cell viability and growth is decreased.
T24 Human Urinary Bladder Cancer Cells, supplied by Coriell Institute for Medical Research, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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( a ) T24 bladder cancer cells, which harbor the c.35G>T mutation, were transfected with HRAS minigenes with either a wild type or an optimized 3’ splice site and treated either with an SSO (SSO-A) that blocks access to the ESE or a scrambled control SSO. SSO-A treatment mediates exon 2 skipping from the wild type HRAS minigene, but this is alleviated when optimizing the 3’ splice site. ( b ) SSO-A treatment causes nearly complete skipping of endogenous HRAS exon 2 in T24 cells. ( c ) Western blot analysis confirmed reduced levels of HRAS protein following SSO-A treatment. ( d ) Quantification of cell viability after SSO-A treatment by WST-1 assay demonstrates that it decreases viability of T24 bladder cancer cells. ( e ) xCelligence real time monitoring of proliferation of T24 bladder cancer cells. Cells were treated with either SSO-A or control SSO at two concentrations (20 nM or 30 nM). When treated with SSO-A cell viability and growth is decreased.

Journal: PLoS Genetics

Article Title: The Splicing Efficiency of Activating HRAS Mutations Can Determine Costello Syndrome Phenotype and Frequency in Cancer

doi: 10.1371/journal.pgen.1006039

Figure Lengend Snippet: ( a ) T24 bladder cancer cells, which harbor the c.35G>T mutation, were transfected with HRAS minigenes with either a wild type or an optimized 3’ splice site and treated either with an SSO (SSO-A) that blocks access to the ESE or a scrambled control SSO. SSO-A treatment mediates exon 2 skipping from the wild type HRAS minigene, but this is alleviated when optimizing the 3’ splice site. ( b ) SSO-A treatment causes nearly complete skipping of endogenous HRAS exon 2 in T24 cells. ( c ) Western blot analysis confirmed reduced levels of HRAS protein following SSO-A treatment. ( d ) Quantification of cell viability after SSO-A treatment by WST-1 assay demonstrates that it decreases viability of T24 bladder cancer cells. ( e ) xCelligence real time monitoring of proliferation of T24 bladder cancer cells. Cells were treated with either SSO-A or control SSO at two concentrations (20 nM or 30 nM). When treated with SSO-A cell viability and growth is decreased.

Article Snippet: T24 human urinary bladder cancer cells were obtained from Coriell Institute ( https://catalog.coriell.org/ ).

Techniques: Mutagenesis, Transfection, Control, Western Blot, WST-1 Assay

( a , b ) HepG2 ( top ) or T24 ( bottom ) cells were transfected with HRAS minigenes harboring different sequence variants in positions c.34-38. The frequencies of the mutations in Costello syndrome according to Giannoulatou and co-workers and in cancer according to Cosmic database are displayed. For cancer the numbers are displayed with skin cancers included or excluded due to the extremely high occurrence of the c.37G>C mutation in skin cancer. The original scoring of the transforming potential of the mutants in two studies are displayed—A is from Seeburg and co-workers ; B is from Fasano and co-workers . Quantitative data for exon 2 inclusion (molar ratio) were obtained from triplicates of duplicate transfections using the Agilent 2100 Bioanalyzer. It is worth noting that there is a clear difference in the overall splicing efficiency between T24 cells and HepG2 cells, which is consistent with the reported low levels of hnRNPF in HepG2 cells .

Journal: PLoS Genetics

Article Title: The Splicing Efficiency of Activating HRAS Mutations Can Determine Costello Syndrome Phenotype and Frequency in Cancer

doi: 10.1371/journal.pgen.1006039

Figure Lengend Snippet: ( a , b ) HepG2 ( top ) or T24 ( bottom ) cells were transfected with HRAS minigenes harboring different sequence variants in positions c.34-38. The frequencies of the mutations in Costello syndrome according to Giannoulatou and co-workers and in cancer according to Cosmic database are displayed. For cancer the numbers are displayed with skin cancers included or excluded due to the extremely high occurrence of the c.37G>C mutation in skin cancer. The original scoring of the transforming potential of the mutants in two studies are displayed—A is from Seeburg and co-workers ; B is from Fasano and co-workers . Quantitative data for exon 2 inclusion (molar ratio) were obtained from triplicates of duplicate transfections using the Agilent 2100 Bioanalyzer. It is worth noting that there is a clear difference in the overall splicing efficiency between T24 cells and HepG2 cells, which is consistent with the reported low levels of hnRNPF in HepG2 cells .

Article Snippet: T24 human urinary bladder cancer cells were obtained from Coriell Institute ( https://catalog.coriell.org/ ).

Techniques: Transfection, Sequencing, Mutagenesis