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: Frontiers in Cellular and Infection Microbiology

Article Title: Activation of the NLRP3 Inflammasome Pathway by Uropathogenic Escherichia coli Is Virulence Factor-Dependent and Influences Colonization of Bladder Epithelial Cells

doi: 10.3389/fcimb.2018.00081

Figure Lengend Snippet: The importance of different virulence factors for IL-1β release and caspase-1 activity. The bladder epithelial cell line 5637 (A–D) and a spontaneously transformed bladder epithelial cell line HBLAK (E) were infected with CFT073, CFT073Δpap, CFT073ΔfimH, CFT073ΔhlyA, CFT073ΔhlyA/pGNH404 and CFT073 fim L-ON at MOI 10 for 3 (A,C) and 6 h (B,D,E) . IL-1β release (A,B,E) and caspase-1 activity (C,D) were measured. Caspase-1 results are presented as fold increase of mean fluorescence units (MFU) compared to unstimulated control cells. Hemolysin activity on blood agar was evaluated for CFT073, CFT073 fim L-ON, and CFT073ΔhlyA after overnight incubation (F) . Data are presented as mean ± SEM ( n = 3 independent experiments). Asterisks denote statistical significance compared to respective unstimulated control (* p < 0.05, ** p < 0.01, *** p < 0.001).

Article Snippet: The human bladder epithelial cell line HBLAK (CELLnTEC Advanced Cell Systems AG, Bern, Switzerland) has been isolated from a healthy bladder and been spontaneously transformed providing the convenience of long-term cell growth without senescence.

Techniques: Activity Assay, Transformation Assay, Infection, Fluorescence, Incubation

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