Microbial Metabolites of Flavanols in Urine are Associated with Enhanced Anti-Proliferative Activity in Bladder Cancer Cells In Vitro

AbstractThe ultimate goal of gene delivery vectors is to establish specific and effective treatments for human diseases. We previously demonstrated that human JC polyomavirus (JCPyV) virus-like particles (VLPs) can package and deliver exogenous DNA into susceptible cells for gene expression. For tissue-specific targeting in this study, JCPyV VLPs were conjugated with a specific peptide for bladder cancer (SPB) that specifically binds to bladder cancer cells. The suicide gene thymidine kinase was packaged and delivered by SPB-conjugated VLPs (VLP-SPBs). Expression of the suicide gene was detected only in human bladder cancer cells and not in lung cancer or neuroblastoma cells susceptible to JCPyV VLP infection in vitro and in vivo, demonstrating the target specificity of VLP-SPBs. The gene transduction efficiency of VLP-SPBs was approximately 100 times greater than that of VLPs without the conjugated peptide. JCPyV VLPs can be specifically guided to target particular cell types when tagged with a ligand molecule that binds to a cell surface marker, thereby improving gene therapy.

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ENHANCED SENSITIVITY OF BLADDER CANCER CELLS TO CISPLATIN MEDIATED CYTOTOXICITY AND APOPTOSIS IN VITRO AND IN VIVO BY THE SELECTIVE CYCLOOXYGENASE-2 INHIBITOR JTE-522

The Journal of Urology ◽

10.1097/01.ju.0000131945.74377.ad ◽

2004 ◽

Vol 172 (4 Part 1) ◽

pp. 1474-1479 ◽

Cited By ~ 18

Author(s):

YOICHI MIZUTANI ◽

HIROYUKI NAKANISHI ◽

YONG NAN LI ◽

NODOKA SATO ◽

AKIHIRO KAWAUCHI ◽

...

Keyword(s):

Bladder Cancer ◽

Cancer Cells ◽

Cyclooxygenase 2 ◽

Enhanced Sensitivity ◽

Bladder Cancer Cells

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Persistent Newcastle disease virus infection in bladder cancer cells is associated with putative pro-survival and anti-viral transcriptomic changes

BMC Cancer ◽

10.1186/s12885-021-08345-y ◽

2021 ◽

Vol 21 (1) ◽

Author(s):

Lee-Chin Chan ◽

Jeevanathan Kalyanasundram ◽

Sze-Wei Leong ◽

Mas Jaffri Masarudin ◽

Abhi Veerakumarasivam ◽

...

Keyword(s):

Bladder Cancer ◽

Newcastle Disease Virus ◽

Cancer Cells ◽

Disease Virus ◽

Newcastle Disease ◽

Persistent Infection ◽

Signalling Pathways ◽

Bladder Cancer Cells ◽

Transcriptomic Changes

Abstract Background Newcastle disease virus (NDV) is an oncolytic virus with excellent selectivity against cancer cells, both in vitro and in vivo. Unfortunately, prolonged in vitro NDV infection results in the development of persistent infection in the cancer cells which are then able to resist NDV-mediated oncolysis. However, the mechanism of persistency of infection remains poorly understood. Methods In this study, we established persistently NDV-infected EJ28 bladder cancer cells, designated as EJ28P. Global transcriptomic analysis was subsequently carried out by microarray analysis. Differentially expressed genes (DEGs) between EJ28 and EJ28P cells identified by the edgeR program were further analysed by Gene Set Enrichment Analysis (GSEA) and Ingenuity Pathway Analysis (IPA) analyses. In addition, the microarray data were validated by RT-qPCR. Results Persistently NDV-infected EJ28 bladder cancer cells were successfully established and confirmed by flow cytometry. Microarray analysis identified a total of 368 genes as differentially expressed in EJ28P cells when compared to the non-infected EJ28 cells. GSEA revealed that the Wnt/β-catenin and KRAS signalling pathways were upregulated while the TGF-β signalling pathway was downregulated. Findings from this study suggest that the upregulation of genes that are associated with cell growth, pro-survival, and anti-apoptosis may explain the survivability of EJ28P cells and the development of persistent infection of NDV. Conclusions This study provides insights into the transcriptomic changes that occur and the specific signalling pathways that are potentially involved in the development and maintenance of NDV persistency of infection in bladder cancer cells. These findings warrant further investigation and is crucial towards the development of effective NDV oncolytic therapy against cancer.

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Parthenolide Induces Apoptosis and Cell Cycle Arrest of Human 5637 Bladder Cancer Cells In Vitro

Molecules ◽

10.3390/molecules16086758 ◽

2011 ◽

Vol 16 (8) ◽

pp. 6758-6768 ◽

Cited By ~ 24

Author(s):

Guang Cheng ◽

Liping Xie

Keyword(s):

Cell Cycle ◽

Bladder Cancer ◽

Cell Cycle Arrest ◽

Cancer Cells ◽

Cycle Arrest ◽

Bladder Cancer Cells

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Olive Mill Wastewater Inhibits Growth and Proliferation of Cisplatin- and Gemcitabine-Resistant Bladder Cancer Cells In Vitro by Down-Regulating the Akt/mTOR-Signaling Pathway

Nutrients ◽

10.3390/nu14020369 ◽

2022 ◽

Vol 14 (2) ◽

pp. 369

Author(s):

Jochen Rutz ◽

Sebastian Maxeiner ◽

Eva Juengel ◽

Felix K.-H. Chun ◽

Igor Tsaur ◽

...

Keyword(s):

Cell Cycle ◽

Bladder Cancer ◽

Cancer Cells ◽

Olive Mill Wastewater ◽

Mtor Signaling ◽

Beneficial Effects ◽

Cycle Arrest ◽

Bladder Cancer Cells ◽

Olive Mill

Bladder cancer patients whose tumors develop resistance to cisplatin-based chemotherapy often turn to natural, plant-derived products. Beneficial effects have been particularly ascribed to polyphenols, although their therapeutic relevance when resistance has developed is not clear. The present study evaluated the anti-tumor potential of polyphenol-rich olive mill wastewater (OMWW) on chemo-sensitive and cisplatin- and gemcitabine-resistant T24, RT112, and TCCSUP bladder cancer cells in vitro. The cells were treated with different dilutions of OMWW, and tumor growth and clone formation were evaluated. Possible mechanisms of action were investigated by evaluating cell cycle phases and cell cycle-regulating proteins. OMWW profoundly inhibited the growth and proliferation of chemo-sensitive as well as gemcitabine- and cisplatin-resistant bladder cancer cells. Depending on the cell line and on gemcitabine- or cisplatin-resistance, OMWW induced cell cycle arrest at different phases. These differing phase arrests were accompanied by differing alterations in the CDK-cyclin axis. Considerable suppression of the Akt-mTOR pathway by OMWW was observed in all three cell lines. Since OMWW blocks the cell cycle through the manipulation of the cyclin-CDK axis and the deactivation of Akt-mTOR signaling, OMWW could become relevant in supporting bladder cancer therapy.

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Evaluation of Su Fu’ning Lotion’s Inhibitory Effects on Bladder Cancer Cells In Vitro and In Vivo by Intravesical Instillation

Integrative Cancer Therapies ◽

10.1177/1534735415596569 ◽

2015 ◽

Vol 15 (1) ◽

pp. 80-86 ◽

Cited By ~ 1

Author(s):

Liansheng Ren ◽

Xihua Yang ◽

Lili Zhao ◽

Hong Zhang ◽

Jing Wang

Keyword(s):

Bladder Cancer ◽

Cancer Cells ◽

Intravesical Instillation ◽

Inhibitory Effects ◽

Bladder Cancer Cells

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DEPDC1B is a tumor promotor in development of bladder cancer through targeting SHC1

Cell Death and Disease ◽

10.1038/s41419-020-03190-6 ◽

2020 ◽

Vol 11 (11) ◽

Author(s):

Chin-Hui Lai ◽

Kexin Xu ◽

Jianhua Zhou ◽

Mingrui Wang ◽

Weiyu Zhang ◽

...

Keyword(s):

Bladder Cancer ◽

Cancer Cells ◽

Malignant Tumors ◽

Tumor Grade ◽

In Vivo Studies ◽

Mechanistic Study ◽

Tumor Promotor ◽

Bladder Cancer Cells

AbstractBladder cancer is one of the most commonly diagnosed malignant tumors in the urinary system and causes a massive cancer-related death. DEPDC1B is a DEP domain-containing protein that has been found to be associated with a variety of human cancers. This study aimed to explore the role and mechanism of DEPDC1B in the development of bladder cancer. The analysis of clinical specimens revealed the upregulated expression of DEPDC1B in bladder cancer, which was positively related to tumor grade. In vitro and in vivo studies showed that DEPDC1B knockdown could inhibit the growth of bladder cancer cells or xenografts in mice. The suppression of bladder cancer by DEPDC1B was executed through inhibiting cell proliferation, cell migration, and promoting cell apoptosis. Moreover, a mechanistic study found that SHC1 may be an important route through which DEPDC1B regulates the development of bladder cancer. Knockdown of SHC1 in DEPDC1B-overexpressed cancer cells could abolish the promotion effects induced by DEPDC1B. In conclusion, DEPDC1B was identified as a key regulator in the development of bladder cancer, which may be used as a potential therapeutic target in the treatment of bladder cancer.

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