Molecular characterization of temsirolimus-induced response in human renal and bladder cancer cell lines.

2012 ◽  
Vol 30 (5_suppl) ◽  
pp. 295-295
Author(s):  
Axel S. Merseburger ◽  
Mario W. Kramer ◽  
Hossein Tezval ◽  
Markus Kuczyk ◽  
Juergen Serth
Keyword(s):  
Bladder Cancer ◽  
Real Time ◽  
Cell Lines ◽  
Cancer Cell ◽  
Expression Patterns ◽  
Impedance Analysis ◽  
Bladder Cancer Cell ◽  
Tumor Entities

295 Background: Targeted therapies like mTOR inhibition is a clinically esthablished treatment modality for advanced renal cell cancer (RCC). We hypothesize that common elements of molecular signalling exists in RCC and transitional cell carcinoma of the bladder (TCC) that could provide a rational of the usage of this novel compound in human TCC. Therefore the goal of this investigation was to measure the in vivo and in vitro effect of temsirolimus/CCI-779 on human RCC and TCC cell lines on the molecular level. Methods: For in vivo experiments 3 RCC (786-O, A498, ACHN) cell lines and 7 TCC (T24, 5637, RT112, EJ-28, CLS-439, HB-CLS-1, HB-CLS-2) cell lines were compared. Effect of temsirolimus/CCI-779 was measured by real time impedance analysis (XCelligence, Roche). Following mRNA isolation microarray based mRNA expression analysis with 45.015 oligoprobes (G4112F, Agilent Technologies) was performed for molecular comparison of RCC and TCC cell lines. Expression patterns of 15 pathways were analyzed using the statistical software R (2.12.0) and the LIMMA package. Results: RCC and TCC cell lines demonstrated dose dependent inhibition of cellular growth with IC50 values of 10-20nM of temsirolimus/CCI-779 as measured by quantitative real time impedance analysis. Furthermore six out of 15 pathways including the mTOR and VEGF signalling were found with similar expression patterns following treatment with CCI-779 in both tumor entities. Conclusions: In vivo and in vitro analysis of temsirolimus mTOR inhitibtion on human bladder cancer cell lines support the hypothesis that a common molecular architectur exists in both tumor entities suggesting inhibition of mTOR in TCC as a possible target for further experimental therapeutic studies.

Synergistic Antitumor Effects of Fleroxacin With 5-fluorouracil In Vitro and In Vivo for Bladder Cancer Cell Lines

Urology ◽  
2009 ◽  
Vol 74 (6) ◽  
pp. 1370-1376 ◽  
Author(s):  
Toru Nishikawa ◽  
Yasuo Kohjimoto ◽  
Masaya Nishihata ◽  
Shoichi Ebisuno ◽  
Isao Hara
Keyword(s):  
Bladder Cancer ◽  
Cell Lines ◽  
Cancer Cell ◽  
Cancer Cell Lines ◽  
Bladder Cancer Cell ◽  
Antitumor Effects

scholarly journals 19-(Benzyloxy)-19-oxojolkinolide B (19-BJB), an ent-abietane diterpene diepoxide, inhibits the growth of bladder cancer T24 cells through DNA damage

PLoS ONE ◽  
2021 ◽  
Vol 16 (3) ◽  
pp. e0248468
Author(s):  
Ke Wang ◽  
Juan-Cheng Yang ◽  
Yeong-Jiunn Jang ◽  
Guan-Yu Chen ◽  
Ya-Jing Zhang ◽  
...  
Keyword(s):  
Dna Damage ◽  
Bladder Cancer ◽  
Cell Lines ◽  
Cancer Cell ◽  
3D Qsar ◽  
Cancer Cell Lines ◽  
Bladder Cancer Cell ◽  
Checkpoint Kinase

Diterpenoids jolkinolide A and B, were first isolated from Euphorbia fischeriana. In our previous research, 19-(Benzyloxy)-19-oxojolkinolide B (19-BJB), a derivative of jolkinolides, was synthesized as a novel ent -abietane diterpene diepoxide. In this study, 19-BJB showed strong in vitro activity against bladder cancer cell lines. DNA damage which was observed through the interaction of 19-BJB with nucleotide chains and affected DNA repair resulted in the activation of checkpoint kinase 1 (Chk1) and checkpoint kinase 2 (Chk2) in bladder cancer cell lines. In vivo testing in nude mice also proved that 19-BJB revealed a potential inhibitory effect on tumor growth. Additionally, the 3D-QSAR models of jolkinolides were established. Briefly, we proved that 19-BJB could potentially be used as a drug to inhibit the growth of bladder tumor.

scholarly journals Comet assay measures of DNA damage are predictive of bladder cancer cell treatment sensitivity in vitro and outcome in vivo

2013 ◽  
Vol 134 (5) ◽  
pp. 1102-1111 ◽  
Author(s):  
Karen J. Bowman ◽  
Manar M. Al‐Moneef ◽  
Benedict T. Sherwood ◽  
Alexandra J. Colquhoun ◽  
Jonathan C. Goddard ◽  
...  
Keyword(s):  
Dna Damage ◽  
Bladder Cancer ◽  
Comet Assay ◽  
Cancer Cell ◽  
Bladder Cancer Cell ◽  
Treatment Sensitivity

scholarly journals In vitro Assessment of Intra-operative and Post-operative Environment in Reducing Bladder Cancer Recurrence

2021 ◽  
Author(s):  
Ryan Tsz-Hei TSE ◽  
Hongda ZHAO ◽  
Christine Yim-Ping WONG ◽  
Angel Wing-Yan KONG ◽  
Ronald Cheong-Kin CHAN ◽  
...  
Keyword(s):  
Bladder Cancer ◽  
Recurrence Rate ◽  
Cell Lines ◽  
Cancer Cell ◽  
Cancer Recurrence ◽  
Bladder Cancer Cell ◽  
Sterile Water ◽  
Cytotoxic Effects ◽  
Bladder Cancer Recurrence

Abstract Urinary bladder cancer is a common cancer worldwide. Currently, the modality of treating and monitoring bladder cancer is wide. Nonetheless, the high recurrence rate of non-muscle-invasive bladder cancer after surgical resection is still unsatisfactory. Hereby, our study demonstrated whether the intra-operative and post-operative environments will affect bladder cancer recurrence utilizing in vitro cell line model. Bladder cancer cell lines were submerged in four different irrigating fluids for assessing their tumorigenic properties. Our results showed that sterile water performed the best in terms of the magnitude of cytotoxicity to cell lines. Besides, we also investigated cytotoxic effects of the four irrigating agents as well as mitomycin C (MMC) in normothermic and hyperthermic conditions. We observed that sterile water and MMC had an increased cytotoxic effects to bladder cancer cell lines in hyperthermic conditions. Altogether, our results could be translated into clinical practice in the future by manipulating the intra-operative and post-operative conditions in order to lower the chance of residual cancer cell reimplant onto the bladder, which in turns, reducing the recurrence rate of bladder cancers.

scholarly journals The lncRNA DLX6-AS1 promoted cell proliferation, invasion, migration and epithelial-to-mesenchymal transition in bladder cancer via modulating Wnt/β-catenin signaling pathway

2019 ◽  
Vol 19 (1) ◽  
Author(s):  
Jinan Guo ◽  
Zhixin Chen ◽  
Hongtao Jiang ◽  
Zhou Yu ◽  
Junming Peng ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Bladder Cancer ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Cancer Progression ◽  
Bladder Cancer Cell ◽  
Mesenchymal Transition ◽  
Bladder Cancer Cells

Abstract Background Bladder cancer is the most common human urological malignancies with poor prognosis, and the pathophysiology of bladder cancer involves multi-linkages of regulatory networks in the bladder cancer cells. Recently, the long noncoding RNAs (lncRNAs) have been extensively studied for their role on bladder cancer progression. In this study, we evaluated the expression of DLX6 Antisense RNA 1 (DLX6-AS1) in the cancerous bladder tissues and studied the possible mechanisms of DLX6-AS1 in regulating bladder cancer progression. Methods Gene expression was determined by qRT-PCR; protein expression levels were evaluated by western blot assay; in vitro functional assays were used to determine cell proliferation, invasion and migration; nude mice were used to establish the tumor xenograft model. Results Our results showed the up-regulation of DLX6-AS1 in cancerous bladder cancer tissues and bladder cell lines, and high expression of DLX6-AS1 was correlated with advance TNM stage, lymphatic node metastasis and distant metastasis. The in vitro experimental data showed that DLX6-AS1 overexpression promoted bladder cancer cell growth, proliferation, invasion, migration and epithelial-to-mesenchymal transition (EMT); while DLX6-AS1 inhibition exerted tumor suppressive actions on bladder cancer cells. Further results showed that DLX6-AS1 overexpression increased the activity of Wnt/β-catenin signaling, and the oncogenic role of DLX6-AS1 in bladder cancer cells was abolished by the presence of XAV939. On the other hand, DLX6-AS1 knockdown suppressed the activity of Wnt/β-catenin signaling, and the tumor-suppressive effects of DLX6-AS1 knockdown partially attenuated by lithium chloride and SB-216763 pretreatment. The in vivo tumor growth study showed that DLX6-AS1 knockdown suppressed tumor growth of T24 cells and suppressed EMT and Wnt/β-catenin signaling in the tumor tissues. Conclusion Collectively, the present study for the first time identified the up-regulation of DLX6-AS1 in clinical bladder cancer tissues and in bladder cancer cell lines. The results from in vitro and in vivo assays implied that DLX6-AS1 exerted enhanced effects on bladder cancer cell proliferation, invasion and migration partly via modulating EMT and the activity of Wnt/β-catenin signaling pathway.

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