scholarly journals Conditioned medium from Ad-IFN-α-infected bladder cancer and normal urothelial cells is cytotoxic to cancer cells but not normal cells: further evidence for a strong bystander effect

2008 ◽  
Vol 15 (12) ◽  
pp. 817-822 ◽  
Author(s):  
X Zhang ◽  
L Dong ◽  
E Chapman ◽  
W F Benedict
Keyword(s):  
Bladder Cancer ◽  
Cancer Cells ◽  
Conditioned Medium ◽  
Bystander Effect ◽  
Urothelial Cells ◽  
Normal Cells

scholarly journals Combined cytotoxic effect of UV-irradiation and TiO2microbeads in normal urothelial cells, low-grade and high-grade urothelial cancer cells

2015 ◽  
Vol 14 (3) ◽  
pp. 583-590 ◽  
Author(s):  
Roghayeh Imani ◽  
Peter Veranič ◽  
Aleš Iglič ◽  
Mateja Erdani Kreft ◽  
Meysam Pazoki ◽  
...  
Keyword(s):  
Bladder Cancer ◽  
Cancer Cells ◽  
Uv Irradiation ◽  
Cytotoxic Effect ◽  
Urothelial Cancer ◽  
Low Grade ◽  
High Grade ◽  
Urothelial Cells ◽  
Efficient Approach

Paper shows that internalization of the TiO2microbeads followed by the UV-irradiation is an efficient approach for killing cancer urothelial cells. Additionally, differentiation dependent differences in the sensitivity of the cells to the UV-irradiation are shown, and a model of photocatalytic treatment of thein vivobladder cancer is presented.

A New Porphyrin Photosensitizer (PH1008) in Model Membranes, Normal Cells, and Bladder Cancer Cells

1992 ◽  
Vol 148 (4) ◽  
pp. 1338-1340
Author(s):  
Mariano Tolentino ◽  
Tetsuya Okunaka ◽  
Marc L. Eckhäuser ◽  
Hideki Yamamoto ◽  
H. Kato ◽  
...  
Keyword(s):  
Bladder Cancer ◽  
Cancer Cells ◽  
Model Membranes ◽  
Normal Cells ◽  
Bladder Cancer Cells

scholarly journals Elevated MCOLN1 Expression in p53-Deficient Bladder Cancer is Necessary for Oncogene-Induced Cell proliferation, Inflammation, and Invasion

2020 ◽  
Author(s):  
Jewon Jung ◽  
Han Liao ◽  
Hong Liang ◽  
John F. Hancock ◽  
Catherine Denicourt ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Bladder Cancer ◽  
Tumor Suppressor ◽  
Cancer Cells ◽  
Therapeutic Strategy ◽  
Cytokine Production ◽  
Urothelial Cells ◽  
Tumor Suppressor P53 ◽  
Wild Type ◽  
Bladder Cancer Cells

SummaryInhibition of the endolysosomal cation channel, TRPML1, which is encoded by MCOLN1, deters the proliferation of cancer cells with augmented TFEB activity. Here, we report that the tumor suppressor, p53, antagonizes TFEB-driven MCOLN1 expression in bladder cancer. Not only was the constitutive loss of p53 in bladder cancer cells associated with higher MCOLN1 mRNA, knockdown of TP53 in lines with wild type alleles of the tumor suppressor increased MCOLN1 expression. Elevated TRPML1 abundance in p53-deficient cancer cells, although not sufficient for bolstering proliferation, was necessary for the effects of oncogenic HRAS on cell division, cytokine production, and invasion. These data demonstrate that hyperactivation of the TFEB– MCOLN1 transcriptional axis in urothelial cells lacking p53 permits tumorigenesis stemming from HRAS mutations. Furthermore, the insight that loss of p53 predicts addiction to TRPML1 informs an actionable therapeutic strategy for bladder cancer.

scholarly journals THE EFFECT OF CONDITIONED-MEDIUM HUMAN ADIPOSE-DERIVED MESENCHYMAL STEM CELL IN APOPTOSIS OF BLADDER CANCER CELLS

2021 ◽  
Vol 28 (1) ◽  
pp. 19-24
Author(s):  
Ari Alauddin Mawdudi ◽  
Furqan Hidayatullah ◽  
Indra Bachtiar ◽  
Arif Rachman ◽  
Indri Lakhsmi Putri ◽  
...  
Keyword(s):  
Stem Cells ◽  
Bladder Cancer ◽  
Mesenchymal Stem Cells ◽  
Cancer Cells ◽  
Conditioned Medium ◽  
Culture Medium ◽  
Entire Study ◽  
Significant Difference ◽  
Bladder Cancer Cells ◽  
Late Apoptosis

Objective: To determine the effect of conditioned medium human Adipose-Derived Mesenchymal Stem Cells (CM-hADMSC) on apoptosis of urothelial bladder cancer cells. Material & Methods: Bladder (5637) cancer cell lines cultured in conditioned media harvested from human adipose-derived mesenchymal stem cells (hADMSC). Flow cytometry tests were carried out using the Flowcytometry Acquisition cell sorting (FACS) Calibur to measure apoptosis. Results: There was a significant difference in the percentage of late apoptosis in the group receiving culture medium treatment: CM-hADMSC 1: 1 to the entire study group. Further analysis revealed no difference in the average percentage of late apoptosis in groups exposed to culture medium: CM-hADMSC 1: 2 and culture medium: CM-hADMSC 1: 4 (p> 0.05). Conclusion: CM-hADMSC at a 1: 1 dose concentration to culture medium obtain a significant increase of apoptosis in bladder cancer cells.

scholarly journals Detrimental Effect of Various Preparations of the Human Amniotic Membrane Homogenate on the 2D and 3D Bladder Cancer In vitro Models

2021 ◽  
Vol 9 ◽  
Author(s):  
Aleksandar Janev ◽  
Taja Železnik Ramuta ◽  
Larisa Tratnjek ◽  
Žiga Sardoč ◽  
Hristina Obradović ◽  
...  
Keyword(s):  
Bladder Cancer ◽  
Cancer Cells ◽  
Amniotic Membrane ◽  
Detrimental Effect ◽  
Human Amniotic Membrane ◽  
Urothelial Cells ◽  
Papillary Cancer ◽  
Cancer Models ◽  
Bladder Cancer Cells ◽  
2D And 3D

Despite being among the ten most common cancers with high recurrence rates worldwide, there have been no major breakthroughs in the standard treatment options for bladder cancer in recent years. The use of a human amniotic membrane (hAM) to treat cancer is one of the promising ideas that have emerged in recent years. This study aimed to investigate the anticancer activity of hAM homogenate on 2D and 3D cancer models. We evaluated the effects of hAM homogenates on the human muscle invasive bladder cancer urothelial (T24) cells, papillary cancer urothelial (RT4) cells and normal porcine urothelial (NPU) cells as well as on human mammary gland non-tumorigenic (MCF10a) cells and low-metastatic breast cancer (MCF7) cells. After 24 h, we observed a gradual detachment of cancerous cells from the culture surface, while the hAM homogenate did not affect the normal cells. The most pronounced effect hAM homogenate had on bladder cancer cells; however, the potency of their detachment was dependent on the treatment protocol and the preparation of hAM homogenate. We demonstrated that hAM homogenate significantly decreased the adhesion, growth, and proliferation of human bladder invasive and papillary cancer urothelial cells and did not affect normal urothelial cells even in 7-day treatment. By using light and electron microscopy we showed that hAM homogenate disrupted the architecture of 2D and 3D bladder cancer models. The information provided by our study highlights the detrimental effect of hAM homogenate on bladder cancer cells and strengthens the idea of the potential clinical application of hAM for bladder cancer treatment.

FOXO1 as a tumor suppressor inactivated via AR/ERβ signals in urothelial cells

2020 ◽  
Vol 27 (4) ◽  
pp. 231-244 ◽  
Author(s):  
Hiroki Ide ◽  
Taichi Mizushima ◽  
Guiyang Jiang ◽  
Takuro Goto ◽  
Yujiro Nagata ◽  
...  
Keyword(s):  
Bladder Cancer ◽  
Tumor Suppressor ◽  
Cancer Cells ◽  
Urothelial Cancer ◽  
Neoplastic Transformation ◽  
Migration And Invasion ◽  
Urothelial Cells ◽  
Estradiol Treatment ◽  
Downstream Target ◽  
Bladder Cancer Cells

Androgen receptor (AR) and estrogen receptor-β (ERβ) have been implicated in urothelial tumor outgrowth as promoters, while underlying mechanisms remain poorly understood. Our transcription factor profiling previously performed identified FOXO1 as a potential downstream target of AR in bladder cancer cells. We here investigated the functional role of FOXO1 in the development and progression of urothelial cancer in relation to AR and ERβ signals. In non-neoplastic urothelial SVHUC cells or bladder cancer lines, AR/ERβ expression or dihydrotestosterone/estradiol treatment reduced the expression levels of FOXO1 gene and induced those of a phosphorylated inactive form of FOXO1 (p-FOXO1). In chemical carcinogen-induced models, FOXO1 knockdown via shRNA or inhibitor treatment resulted in considerable induction of the neoplastic transformation of urothelial cells or bladder cancer development in mice. Similarly, FOXO1 inhibition considerably induced the viability, migration, and invasion of bladder cancer cells. Importantly, in FOXO1 knockdown sublines, an anti-androgen hydroxyflutamide or an anti-estrogen tamoxifen did not significantly inhibit the neoplastic transformation of urothelial cells, while dihydrotestosterone or estradiol did not significantly promote the proliferation or migration of urothelial cancer cells. In addition, immunohistochemistry in surgical specimens showed that FOXO1 and p-FOXO1 expression was down-regulated and up-regulated, respectively, in bladder tumor tissues, which was further associated with worse patient outcomes. AR or ERβ activation is thus found to correlate with inactivation of FOXO1 which appears to be their key downstream effector. Moreover, FOXO1, as a tumor suppressor, is likely inactivated in bladder cancer, which contributes in turn to inducing urothelial carcinogenesis and cancer growth.

Hypoxia and Proton microbeam: Role of Gap Junction Intercellular Communication in Inducing Bystander Responses on Human Lung Cancer Cells and Normal Cells

2022 ◽  
Author(s):  
Narongchai Autsavapromporn ◽  
Alisa Kobayashi ◽  
Cuihua Liu ◽  
Churdsak Jaikang ◽  
Tengku Ahbrizal Tengku Ahmad ◽  
...  
Keyword(s):  
Gap Junction ◽  
Cancer Cells ◽  
Intercellular Communication ◽  
Bystander Effect ◽  
A549 Cells ◽  
Human Lung Cancer ◽  
Tumor Resistance ◽  
Normal Cells ◽  
Gap Junction Intercellular Communication ◽  
High Let

Radiation-induced bystander effect (RIBE) has been identified as an important contributing factor to tumor resistance and normal tissue damage. However, the RIBE in cancer and normal cells under hypoxia remain unclear. In this study, confluent A549 cancer and WI-38 normal cells were subjected to condition of hypoxia or normoxia, before exposure to high-LET protons microbeam. After 6 h incubation, cells were harvested and assayed for colony formation, micronucleus formation, chromosome aberration and western blotting. Our results show that there were differences of RIBE in bystander A549 and WI-38 cells under hypoxia and normoxia. The differences were also observed in the roles of HIF-1α expression in bystander A549 and WI-38 cells under both conditions. Furthermore, inhibition of gap junction intercellular communication (GJIC) showed a decrease in toxicity of hypoxia-treated bystander A549 cells, but increased in bystander WI-38 cells. These findings clearly support that GJIC protection of bystander normal cells from toxicity while enhancing in bystander cancer cells. Together, the data show a promising strategy for high-LET radiation in designing an entire new line of drugs, either increase or restore GJIC in bystander cancer cells which in turn leads to enhancement of radiation accuracy for treatment of hypoxic tumors.

758: Inflammatory and Anti-Inflammatory Regulators alter Levels of an Inhibitor of Apoptosis (IAP), Survivin, in T-24 Bladder Cancer Cells

2007 ◽  
Vol 177 (4S) ◽  
pp. 254-254
Author(s):  
Justin J. Cohen ◽  
Bayan T. Takizawa ◽  
Hristos Z. Kaimkliotis ◽  
David J. Rosenberg ◽  
Marcia A. Wheeler ◽  
...  
Keyword(s):  
Bladder Cancer ◽  
Cancer Cells ◽  
Inhibitor Of Apoptosis ◽  
Bladder Cancer Cells ◽  
Anti Inflammatory

792: Role of Oxidative Stress in Tumorigenic Potential of Bladder Cancer Cells

2005 ◽  
Vol 173 (4S) ◽  
pp. 214-215 ◽  
Author(s):  
Daniel Cho ◽  
Xiao Fang Ha ◽  
J. Andre Melendez ◽  
Louis J. Giorgi ◽  
Badar M. Mian
Keyword(s):  
Oxidative Stress ◽  
Bladder Cancer ◽  
Cancer Cells ◽  
Tumorigenic Potential ◽  
Bladder Cancer Cells
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