Rapid bladder cancer cell detection from clinical urine samples using an ultra-thin silicone membrane

The Analyst ◽  
2016 ◽  
Vol 141 (2) ◽  
pp. 652-660 ◽  
Author(s):  
Jennie H. Appel ◽  
Hao Ren ◽  
Mandy L. Y. Sin ◽  
Joseph C. Liao ◽  
Junseok Chae
Keyword(s):  
Bladder Cancer ◽  
Cancer Cells ◽  
Cancer Cell ◽  
High Throughput ◽  
Urine Samples ◽  
Cell Detection ◽  
Silicone Membrane ◽  
Bladder Cancer Cells ◽  
Cancer Cell Detection ◽  
Cancerous Cells

A high-throughput strategy capable of differentiating bladder cancer cells from non-cancerous cells based on their respective cellular traction forces.

Apoptosis triggered by isoquercitrin in bladder cancer cells by activating the AMPK-activated protein kinase pathway

2017 ◽  
Vol 8 (10) ◽  
pp. 3707-3722 ◽  
Author(s):  
Ping Wu ◽  
Siyuan Liu ◽  
Jianyu Su ◽  
Jianping Chen ◽  
Lin Li ◽  
...  
Keyword(s):  
Bladder Cancer ◽  
Protein Kinase ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Cell Metabolism ◽  
Bladder Cancer Cell ◽  
Bladder Cancer Cells ◽  
Immunoblotting Assay ◽  
Cancer Cell Metabolism ◽  
Kinase Pathway

Our findings provide comprehensive evidence that isoquercitrin (ISO) influenced T24 bladder cancer cell metabolism by activating the AMPK pathway as identified by combination with metabolomics and immunoblotting assay.

Cancer cell detection device for the diagnosis of bladder cancer from urine

2021 ◽  
Vol 171 ◽  
pp. 112699
Author(s):  
Melanie MacGregor ◽  
Hanieh Safizadeh Shirazi ◽  
Kit Man Chan ◽  
Kola Ostrikov ◽  
Kym McNicholas ◽  
...  
Keyword(s):  
Bladder Cancer ◽  
Cancer Cell ◽  
Cell Detection ◽  
Cancer Cell Detection

scholarly journals Design of MEMS-based Microfludic Channel to Detect Cancer Cells in Blood

2020 ◽  
Vol 11 (1) ◽  
pp. 561-566
Author(s):  
Syed Shameem ◽  
RamaKrishna T V ◽  
Sahithi M ◽  
Rohitha B ◽  
Keerthana J ◽  
...  
Keyword(s):  
Cancer Cells ◽  
Cancer Cell ◽  
Early Stage ◽  
Microfluidic Channel ◽  
Cell Detection ◽  
Malignant Growth ◽  
Simple Manner ◽  
Abnormal Cells ◽  
Mass Displacement ◽  
Cancer Cell Detection

Cancer refers to any of countless infections characterized by the development of abnormal cells that divide uncontrollably and can invade and destroy normal body tissue. Malignant growth frequently can spread all through your body. Cancer is the second driving reason for death on the planet. In this paper, we propose to found a H-cell to screen carcinogenic cells in a given sample of blood based on the principle of diffusion. This model incorporates the planning of a MEMS-based microfluidic channel to screen and recognize different cells depending on the size and various characteristics of the cells. Some of the methods which are implemented not efficient models for cancer cells detection in blood. The mass, displacement technique has been implemented in this investigation for cancer cell detection, with the help of this achieves the accuracy and better throughput. One cancer cell contains = 1.70371e-24 mass, such that with a weight of this formula, find out the total no of cells in the blood. This is the best method compared to existed methods. Using this count, the weight has been calculate early-stage cancer and treatment with a simple manner, CTCs in the blood is the un potential matter for health, H-cells have been measured with proposed weight and force technique such that in this investigation also calculate the healthy and cancer cells also. Finally, using this methodology achieves 93.58% accuracy, 0.00124 MSE. These are very good results compared to conventional methods.

scholarly journals TRAF4 inhibits bladder cancer progression by promoting BMP/SMAD signalling pathway

2020 ◽  
Author(s):  
Prasanna Vasudevan Iyengar ◽  
Dieuwke Louise Marvin ◽  
Dilraj Lama ◽  
Tuan Zea Tan ◽  
Sudha Suriyamurthy ◽  
...  
Keyword(s):  
Bladder Cancer ◽  
Cancer Cells ◽  
Cell Lines ◽  
Cancer Cell ◽  
Ubiquitin Ligase ◽  
E3 Ubiquitin Ligase ◽  
Cancer Cell Lines ◽  
Bladder Cancer Cell ◽  
Over Expression ◽  
Bladder Cancer Cells

AbstractBladder cancer is one of the most prevalent cancer types in the world, frequently exhibiting invasion and metastasis and therefore associated with poor prognosis. It is a progressive disease with high recurrence rates even after surgery, which calls for the urgent need for early intervention and diagnosis. The E3 ubiquitin ligase TNF Receptor Associated Factor 4 (TRAF4) has been largely implicated as a tumour-promoting element in a wide range of cancers. Over-expression and amplification of this gene product has been a common observation in breast and other metastatic tumours. In contrast, we observed that expression of TRAF4 negatively correlated with overall patient survival. Moreover, its expression was repressed at epigenetic levels in aggressive bladder cancer cells. We also describe an ERK kinase phosphorylation site on TRAF4 that inhibits its stability and localization to plasma membrane in such cells. Furthermore, knockdown of TRAF4 in epithelial bladder cancer cell lines leads to gain of mesenchymal genes and a loss of epithelial integrity. Reciprocally, stable over-expression of TRAF4 in mesenchymal cells leads to decreased migratory and invasive properties. Transcriptomic analysis upon TRAF4 mis-expression in bladder cancer cell lines revealed that higher TRAF4 expression enhanced BMP/SMAD and dampened NF-κB signalling pathways. Importantly, this notion was confirmed in bladder cancer patient material. Mechanistically, we showed that TRAF4 targets the E3 ubiquitin ligase SMURF1, a negative regulator of BMP/SMAD signalling, for proteasomal degradation in bladder cancer cells. We show that genetic and pharmacological inhibition of SMURF1 or its function inhibited migration of aggressive (mesenchymal) bladder cancer cells.

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.

Glucose metabolism and bladder cancer.

2017 ◽  
Vol 35 (6_suppl) ◽  
pp. 359-359
Author(s):  
Eugene K. Lee ◽  
Karim Pirani ◽  
Jeffrey M. Holzbeierlein ◽  
Paige Martin ◽  
Parthasarathy Rangarajan ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Bladder Cancer ◽  
Glucose Metabolism ◽  
Cancer Cells ◽  
Glucose Concentration ◽  
Tca Cycle ◽  
Urine Samples ◽  
Pcr Array ◽  
Elisa Kit ◽  
Bladder Cancer Cells

359 Background: To understand and evaluate the role of glucose metabolism in bladder cancer growth, in the identification of disease, and development of potential treatment strategies. Methods: UMUC3, T24 and 253JBV cells were grown in varying glucose concentrations (25, 100 and 200mg/dl) and cell proliferation assay with Vi-Cell was performed. Next, we used Qiagen PCR array of glucose metabolic pathway of the UMUC3 cell line under different glucose concentrations. PKM2 is a driver of glycolysis and exists in an inactive dimer or active tetramer. Dimer PKM2 also known as Tumor M2-PK was measured in urine samples of bladder cancer patients using a commercially available ELISA kit (ScheBo Biotech AG). Lastly, Shikonin, a PKM2 inhibitor was evaluated as an inhibitor of bladder cancer cell proliferation using Vi-Cell. Results: Increased glucose concentration 200mg/dl leads to increased proliferation in bladder cancer cells while decreased concentration of glucose; 25mg/dl reduces proliferation compared to control (100). PCR array demonstrates genes in the glycolytic pathway genes are upregulated in cells that are grown in 200mg/dl glucose media and the TCA cycle genes are upregulated in cells that are subjected to the 25mg/dl glucose media when compared to control (100mg/dl). The enzyme pyruvate kinase M2 (PKM2) controls the transition from the glycolytic pathway to TCA cycle. We have found that 9/10 (90%) of bladder cancer urine samples show elevated levels of tumor M2-PK (>104) compared to urine from two normal subjects (~30 units ) using a commercially available ELISA kit. Conclusions: Increased glucose concentration 200mg/dl leads to increased proliferation in bladder cancer cells while decreased concentration of glucose; 25mg/dl reduces proliferation compared to control (100).

scholarly journals Chloride Ion Transport Blockade Enhances Cytocidal Effects of Sterile Water on Bladder Cancer Cells

2021 ◽  
Author(s):  
Yuki Matsuoka ◽  
Rikiya Taoka ◽  
Yoichiro Tohi ◽  
Zhang Xia ◽  
Mikio Sugimoto
Keyword(s):  
Bladder Cancer ◽  
Cancer Cells ◽  
Cell Lines ◽  
Cancer Cell ◽  
Channel Blocker ◽  
Bladder Cancer Cell ◽  
Channel Blockers ◽  
Sterile Water ◽  
Hypotonic Shock ◽  
Bladder Cancer Cells

Abstract Background:Bladder cancer is a major health concern worldwide. The conventional intravesical Bacillus Calmette–Guérin therapy has certain shortcomings; thereby, demanding novel alternatives. Although sterile water is a probable agent for such novel intravesical therapies, bladder cancer cell lines differ in their sensitivity to hypotonic shock due to sterile water. Therefore, we aimed to investigate whether Cl- channel blockers enhance the cytocidal effect of hypotonic shock on bladder cancer cells resistant to sterile water.Methods:Bladder cancer cell lines of varying grades (RT112, T24, and J82) were exposed to sterile water, and morphological changes were closely observed using microscopy. Sterile water-induced changes in cell membrane integrity and cell viability were analyzed to determine the effects of hypotonic shock. These effects were further analyzed using a Cl- channel blocker.Results:T24 and J82 cells started swelling immediately upon exposure to sterile water and ruptured within 10 min. RT112 cells demonstrated limited hypotonic swelling with few cell ruptures. After treatment with the Cl- channel blocker, RT112 cells ruptured faster as compared to that in cells treated with sterile water. The percentages of viable dimethylsulfoxide and 5-nitro-2-(3-phenylpropylamino) benzoic acid -treated (50, 100, 200, and 300 µM) RT112 cells after 10 min of exposure to sterile water were 13.6 % ± 3.4 %, 6.3 % ± 1.2 %, 2.0 % ± 1.1 %, 0.7 % ± 0.7 %, and 0 %, respectively.Conclusions:Taken together, the Cl- channel blockers enhanced the cytocidal effects of hypotonic shock in bladder cancer cells. Intravesical therapy with sterile water after treatment with a Cl- channel blocker represents a potential new adjuvant therapy after TURBT with high efficacy.

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