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: Silencing of ECHDC1 inhibits growth of gemcitabine-resistant bladder cancer cells

doi: 10.3892/ol.2017.7269

Figure Lengend Snippet: Analysis of gemcitabine resistance of the bladder cancer cell lines. Bladder cancer cells were treated with gemcitabine for 72 h and cell viability was analyzed using CCK-8. The viability of parental UMUC3 (A) and HT1376 (B) cells was respectively suppressed compared to (A) UMUC3GR and (B) HT1376GR by treatment with gemcitabine in a dose-dependent manner. Values are expressed as means ± standard deviation.

Article Snippet: Cell culture The human bladder cancer cell lines, UMUC3 and HT1376, which were used in this study, were purchased from DS Pharma Biomedical (Osaka, Japan).

Techniques: CCK-8 Assay, Standard Deviation

Journal: Oncology Letters

Article Title: Silencing of ECHDC1 inhibits growth of gemcitabine-resistant bladder cancer cells

doi: 10.3892/ol.2017.7269

Figure Lengend Snippet: Proteins with increased expression in gemcitabine-resistant cells identified using iTRAQ proteomic analysis.

Article Snippet: Cell culture The human bladder cancer cell lines, UMUC3 and HT1376, which were used in this study, were purchased from DS Pharma Biomedical (Osaka, Japan).

Techniques: Expressing, Multiplex sample analysis, Histone Deacetylase Assay

Journal: Oncology Letters

Article Title: Silencing of ECHDC1 inhibits growth of gemcitabine-resistant bladder cancer cells

doi: 10.3892/ol.2017.7269

Figure Lengend Snippet: ECHDC1 protein expression in gemcitabine resistant and sensitive cell lines. (A) ECHDC1 protein expression levels in parental and gemcitabine resistant (GR) cell lines were determined using western blotting. ECHDC1 expression levels were clearly increased in the gemcitabine-resistant cells compared to the gemcitabine-sensitive cells. (B) Immunofluorescence analysis of ECHDC1 expression (red) in the indicated cells. Nuclei were counterstained with Hoechst 33342 (blue). The red signal in the cytoplasm, reflecting ECHDC1 expression, was much stronger in UMUC3GR than in UMUC3 cells.

Article Snippet: Cell culture The human bladder cancer cell lines, UMUC3 and HT1376, which were used in this study, were purchased from DS Pharma Biomedical (Osaka, Japan).

Techniques: Expressing, Western Blot, Immunofluorescence

Journal: Pharmaceuticals

Article Title: Trichostatin C Synergistically Interacts with DNMT Inhibitor to Induce Antineoplastic Effect via Inhibition of Axl in Bladder and Lung Cancer Cells

doi: 10.3390/ph17040425

Figure Lengend Snippet: Characterization of TSC of its cytotoxicity and HDAC inhibitory activity. Structure of TSC (TSC) isolated from fermentation of Streptomyces sp. CPCC 203,909 ( a ). Concentration–effect curves of TSC in A549, SK-BR-3, and J82 ( b ). Acetylation levels of α-Tubulin and Histone H3. J82 cells were treated with the indicated concentrations of trichostatin A, Entinostat, and TSC ( c ).

Article Snippet: The human urothelial bladder cancer cell line J82 was obtained from Merck Millipore (Burlington, MA, USA).

Techniques: Activity Assay, Isolation, Concentration Assay

Journal: Pharmaceuticals

Article Title: Trichostatin C Synergistically Interacts with DNMT Inhibitor to Induce Antineoplastic Effect via Inhibition of Axl in Bladder and Lung Cancer Cells

doi: 10.3390/ph17040425

Figure Lengend Snippet: TSC-induced activation of caspase 3/7. J82 cells were treated with TSC with TSC for 48 h and labeled with Hoechst 33,342 for cell nucleus and CellEvent caspase 3/7 reagent for activated caspase 3/7 ( a ). Percentage of caspase 3/7-positive cells ( b ). The two-tailed Student’s t -test or ANOVA was applied. Results are presented as mean ± SEM from three experiments. * p < 0.05 compared to control cells.

Article Snippet: The human urothelial bladder cancer cell line J82 was obtained from Merck Millipore (Burlington, MA, USA).

Techniques: Activation Assay, Labeling, Two Tailed Test

Journal: Pharmaceuticals

Article Title: Trichostatin C Synergistically Interacts with DNMT Inhibitor to Induce Antineoplastic Effect via Inhibition of Axl in Bladder and Lung Cancer Cells

doi: 10.3390/ph17040425

Figure Lengend Snippet: Synergistic anti-cancer effect of TSC and decitabine in human urothelial bladder cancer cell line J82 and human lung cancer cell line A549. Total of 48 h incubation with decitabine prior to TSC significantly increased cytotoxicity of TSC in J82 ( a ) and in A549 ( b ) cell lines. Synergistic effect was determined by the Chou–Talalay method in J82 ( c ) and A549 ( d ) cell lines. Left panel and middle panels: cell survival rate upon treatment with TSC and decitabine alone or in combination. The right panel indicates the fraction of cells affected (Fa) and CI. Synergistic effect is defined by CI < 1. Results are presented as mean ± SD from three experiments. ** p < 0.01, * p < 0.05, combination treatment vs. single treatment.

Article Snippet: The human urothelial bladder cancer cell line J82 was obtained from Merck Millipore (Burlington, MA, USA).

Techniques: Incubation

Journal: Pharmaceuticals

Article Title: Trichostatin C Synergistically Interacts with DNMT Inhibitor to Induce Antineoplastic Effect via Inhibition of Axl in Bladder and Lung Cancer Cells

doi: 10.3390/ph17040425

Figure Lengend Snippet: TSC altered expression of Axl and targets involved in FoxO1 pathway. Representative Western blot analysis of J82 cells upon the treatment of TSC for 48 h ( a ). Densitometrically measure expression of proteins relative to GAPDH are shown with three independent experiments ( b ). Results shown are the mean ± SD from three independent experiments. ** p < 0.01, * p < 0.05 as compared with control cells.

Article Snippet: The human urothelial bladder cancer cell line J82 was obtained from Merck Millipore (Burlington, MA, USA).

Techniques: Expressing, Western Blot

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