Journal: International Journal of Molecular Sciences

Article Title: BMP9 Promotes the Proliferation and Migration of Bladder Cancer Cells through Up-Regulating lncRNA UCA1

doi: 10.3390/ijms19041116

Figure Lengend Snippet: The validation of recombinant adenovirus BMP9 and siBMP9. ( A ) The expression of BMP9 in normal bladder mucosa ( n = 126), superficial bladder cancer ( n = 68), and infiltrating bladder cancer ( n = 62) in the Lee Bladder database. p = 0.007; ( B ) The expression levels of BMP9 in T24 and BIU-87 cells were detected by western blot; ( C ) The BMP9 was up-regulated in BIU-87 cells after being transfected with AdBMP9 compared to the control group; ( D ) The BMP9 was down-regulated in T24 cells after being transfected with AdsiBMP9 compared to the control group. Data are shown as mean ± SD. ** p < 0.01.

Article Snippet: Human bladder cancer BIU-87 and T24 cells were obtained from the China Center for Type Culture Collection (CCTCC).

Techniques: Biomarker Discovery, Recombinant, Expressing, Western Blot, Transfection, Control

Journal: International Journal of Molecular Sciences

Article Title: BMP9 Promotes the Proliferation and Migration of Bladder Cancer Cells through Up-Regulating lncRNA UCA1

doi: 10.3390/ijms19041116

Figure Lengend Snippet: BMP9 up-regulated the expression of lncRNA UCA1 in bladder cancer cells. ( A ) Five common lncRNA were screened in BIU-87 cells after transfected with AdBMP9 by RT-PCR; ( B ) The expression of lncRNA UCA1 were verified in BIU-87 cells after transfected with AdBMP9 by RT-PCR; ( C ) The expression of lncRNA UCA1 were tested in T24 cells after being transfected with AdsiBMP9 by RT-PCR; ( D ) The inhibitory effect of siUCA1 were analyzed by RT-PCR in BIU-87 cells after being co-transfected with AdBMP9 and siUCA1. Data are shown as mean ± SD. ns p > 0.05, * p < 0.05, ** p < 0.01, *** p < 0.001, vs. control groups.

Article Snippet: Human bladder cancer BIU-87 and T24 cells were obtained from the China Center for Type Culture Collection (CCTCC).

Techniques: Expressing, Transfection, Reverse Transcription Polymerase Chain Reaction, Control

Journal: Oncology Letters

Article Title: Cisplatin resistance by induction of aldo-keto reductase family 1 member C2 in human bladder cancer cells

doi: 10.3892/ol.2013.1768

Figure Lengend Snippet: AKR1C2 protein expression in HT1376-CisR cells was markedly increased in comparison with the parental cells. AKR1C2 small interfering RNA reduced expression by ~80% in HT1376-CisR cells. AKR1C2 and β-tubulin exhibit discrete bands of the same molecular weight (AKR1C2, 37 kDa; β-tubulin, 51 kDa). AKR1C2, aldo-keto reductase family 1 member C2; CisR, cisplatin-resistant.

Article Snippet: The human HT1376 bladder cancer cell line used in this study was purchased from DS Pharma Biomedical (Osaka, Japan).

Techniques: Expressing, Comparison, Small Interfering RNA, Molecular Weight

Journal: Oncology Letters

Article Title: Cisplatin resistance by induction of aldo-keto reductase family 1 member C2 in human bladder cancer cells

doi: 10.3892/ol.2013.1768

Figure Lengend Snippet: Effect of AKR1C2 expression on cisplatin IC 50 values in parental and HT1376-CisR cells. Cells were treated with various cisplatin concentrations for 72 h, and then quantified using a cell counter. Each assay was performed in triplicate. Cell survival in the absence of cisplatin was set as 100%. (A) Silencing AKR1C2 restored HT1376-CisR cell response to cisplatin. (B) Inhibition of AKR1C2 by 100 μM 5β-cholanic acid restored the HT1376-CisR response to cisplatin. * P<0.05, vs. HT1376-CisR. Bars indicate standard deviation. AKR1C2, aldo-keto reductase family 1 member C2; CisR, cisplatin-resistant.

Article Snippet: The human HT1376 bladder cancer cell line used in this study was purchased from DS Pharma Biomedical (Osaka, Japan).

Techniques: Expressing, Inhibition, Standard Deviation

Journal: Oncology Letters

Article Title: Cisplatin resistance by induction of aldo-keto reductase family 1 member C2 in human bladder cancer cells

doi: 10.3892/ol.2013.1768

Figure Lengend Snippet: Effect of cisplatin on intracellular ROS in HT1376 cells. Exposure to cisplatin increased the levels of intracellular ROS in HT1376 cells in a dose-dependent manner. * P<0.05, vs. HT1376 cells cultured without cisplatin. Bars indicate standard deviation. ROS, reactive oxygen species.

Article Snippet: The human HT1376 bladder cancer cell line used in this study was purchased from DS Pharma Biomedical (Osaka, Japan).

Techniques: Cell Culture, Standard Deviation

Journal: Oncology Letters

Article Title: Cisplatin resistance by induction of aldo-keto reductase family 1 member C2 in human bladder cancer cells

doi: 10.3892/ol.2013.1768

Figure Lengend Snippet: Relative values of intracellular ROS measured using a 2,7-dichlorodihydrofluorescein diacetate probe. (A) Basal intracellular ROS levels in HT1376, HT1376-CisR and HT1376-CisR cells transiently transfected with AKR1C2 small interfering RNA [HT1376-CisR-AKR1C2(−)]. * P<0.05 and $ P<0.05, vs. HT1376 and HT1376-CisR cells cultured without cisplatin, respectively. (B) Effect of 10 −4 M cisplatin exposure on intracellular ROS in these cells. (C) Effect of 5 μM menadione on intracellular ROS in these cells. * P<0.05 vs. control cells cultured without cisplatin or menadione. Bars indicate standard deviation. AKR1C2, aldo-keto reductase family 1 member C2; CisR, cisplatin-resistant; ROS, reactive oxygen species.

Article Snippet: The human HT1376 bladder cancer cell line used in this study was purchased from DS Pharma Biomedical (Osaka, Japan).

Techniques: Transfection, Small Interfering RNA, Cell Culture, Control, Standard Deviation

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

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