scholarly journals Fangchinoline Induces Apoptosis, Autophagy and Energetic Impairment in Bladder Cancer

2017 ◽  
Vol 43 (3) ◽  
pp. 1003-1011 ◽  
Author(s):  
Bo Fan ◽  
Xiaoyu Zhang ◽  
Yongliang Ma ◽  
Aili Zhang
Keyword(s):  
Bladder Cancer ◽  
Cancer Cells ◽  
Potential Candidate ◽  
Dependent Manner ◽  
Concentration Dependent Manner ◽  
Metabolic Substrates ◽  
Bladder Cancer Cells ◽  
Exogenous Addition ◽  
Induced Apoptosis

Background/Aims: Tetrandrine and Fangchinoline (Fcn) are two natural products that are found in Stephania tetrandra. Tetrandrine is a known anti-bladder cancer compound, but the effects of Fcn on bladder cancer have been previously unclear. In the present study, we focused on the anti-tumor effects of Fcn on bladder cancer. Methods and Results: We treated T24 and 5637 bladder cancer cell lines with Fcn in vitro. We observed that Fcn inhibited the viability of bladder cancer cells in a concentration-dependent manner. The expression of PCNA, a biomarker of proliferation, was down-regulated. Fcn treatment induced both apoptosis and autophagy in bladder cancer cells, as shown by the increased cleavage of caspase-3, an up-regulated LC3-II/LC3-I ratio and the down-regulated p62 level. Blocking autophagy with 3-MA (3-Methyladenine) enhanced Fcn-induced apoptosis, indicating that Fcn-induced autophagy was adaptive. Additionally, we observed that Fcn treatment inhibited mTOR and reduced the intracellular ATP levels. The exogenous addition of methyl pyruvate (MP) to compensate metabolic substrates alleviated Fcn-induced apoptosis and autophagy. Conclusions: Our data indicated that Fcn caused an impairment in energy generation, which led to apoptosis and adaptive autophagy in bladder cancer. These results demonstrated that Fcn may be a potential candidate for use in the prevention and treatment of bladder cancer.

scholarly journals Genistein Sensitizes Bladder Cancer Cells to HCPT Treatment In Vitro and In Vivo via ATM/NF-κB/IKK Pathway-Induced Apoptosis

PLoS ONE ◽  
2013 ◽  
Vol 8 (1) ◽  
pp. e50175 ◽  
Author(s):  
Yong Wang ◽  
He Wang ◽  
Wei Zhang ◽  
Chen Shao ◽  
Peng Xu ◽  
...  
Keyword(s):  
Bladder Cancer ◽  
Cancer Cells ◽  
Bladder Cancer Cells ◽  
Induced Apoptosis

Vitamin E succinate induced apoptosis and enhanced chemosensitivity to paclitaxel in human bladder cancer cells in vitro and in vivo

2010 ◽  
Vol 101 (1) ◽  
pp. 216-223 ◽  
Author(s):  
Kunimitsu Kanai ◽  
Eiji Kikuchi ◽  
Shuji Mikami ◽  
Eriko Suzuki ◽  
Yasumitsu Uchida ◽  
...  
Keyword(s):  
Bladder Cancer ◽  
Vitamin E ◽  
Cancer Cells ◽  
Human Bladder Cancer ◽  
Human Bladder ◽  
Bladder Cancer Cells ◽  
Induced Apoptosis ◽  
Human Bladder Cancer Cells

SYSTEMATIC IN VITRO EVALUATION OF SURVIVIN DIRECTED ANTISENSE OLIGODEOXYNUCLEOTIDES IN BLADDER CANCER CELLS

2004 ◽  
Vol 171 (6 Part 1) ◽  
pp. 2471-2476 ◽  
Author(s):  
SUSANNE FUESSEL ◽  
BERND KUEPPERS ◽  
SHUANGLI NING ◽  
MATTHIAS KOTZSCH ◽  
KAI KRAEMER ◽  
...  
Keyword(s):  
Bladder Cancer ◽  
Cancer Cells ◽  
Antisense Oligodeoxynucleotides ◽  
In Vitro Evaluation ◽  
Bladder Cancer Cells

scholarly journals Peptide-guided JC polyomavirus-like particles specifically target bladder cancer cells for gene therapy

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Wei-Hong Lai ◽  
Chiung-Yao Fang ◽  
Ming-Chieh Chou ◽  
Mien-Chun Lin ◽  
Cheng-Huang Shen ◽  
...  
Keyword(s):  
Gene Therapy ◽  
Bladder Cancer ◽  
Cancer Cells ◽  
Suicide Gene ◽  
Transduction Efficiency ◽  
Ligand Molecule ◽  
Jc Polyomavirus ◽  
Exogenous Dna ◽  
Bladder Cancer Cells

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.

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

2021 ◽  
pp. 1-17
Author(s):  
Laura E. Griffin ◽  
Sarah E. Kohrt ◽  
Atul Rathore ◽  
Colin D. Kay ◽  
Magdalena M. Grabowska ◽  
...  
Keyword(s):  
Bladder Cancer ◽  
Cancer Cells ◽  
Proliferative Activity ◽  
Microbial Metabolites ◽  
Bladder Cancer Cells

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

2004 ◽  
Vol 172 (4 Part 1) ◽  
pp. 1474-1479 ◽  
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

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

BMC Cancer ◽  
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.

scholarly journals Betulinic Acid Restricts Human Bladder Cancer Cell Proliferation In Vitro by Inducing Caspase-Dependent Cell Death and Cell Cycle Arrest, and Decreasing Metastatic Potential

Molecules ◽  
2021 ◽  
Vol 26 (5) ◽  
pp. 1381
Author(s):  
So Young Kim ◽  
Hyun Hwangbo ◽  
Min Yeong Kim ◽  
Seon Yeong Ji ◽  
Da Hye Kim ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Bladder Cancer ◽  
Cell Cycle Arrest ◽  
Cancer Cells ◽  
Human Bladder Cancer ◽  
Human Bladder ◽  
Cycle Arrest ◽  
Bladder Cancer Cells ◽  
Induced Apoptosis ◽  
Human Bladder Cancer Cells

Betulinic acid (BA) is a naturally occurring pentacyclic triterpenoid and generally found in the bark of birch trees (Betula sp.). Although several studies have been reported that BA has diverse biological activities, including anti-tumor effects, the underlying anti-cancer mechanism in bladder cancer cells is still lacking. Therefore, this study aims to investigate the anti-proliferative effect of BA in human bladder cancer cell lines T-24, UMUC-3, and 5637, and identify the underlying mechanism. Our results showed that BA induced cell death in bladder cancer cells and that are accompanied by apoptosis, necrosis, and cell cycle arrest. Furthermore, BA decreased the expression of cell cycle regulators, such as cyclin B1, cyclin A, cyclin-dependent kinase (Cdk) 2, cell division cycle (Cdc) 2, and Cdc25c. In addition, BA-induced apoptosis was associated with mitochondrial dysfunction that is caused by loss of mitochondrial membrane potential, which led to the activation of mitochondrial-mediated intrinsic pathway. BA up-regulated the expression of Bcl-2-accociated X protein (Bax) and cleaved poly-ADP ribose polymerase (PARP), and subsequently activated caspase-3, -8, and -9. However, pre-treatment of pan-caspase inhibitor markedly suppressed BA-induced apoptosis. Meanwhile, BA did not affect the levels of intracellular reactive oxygen species (ROS), indicating BA-mediated apoptosis was ROS-independent. Furthermore, we found that BA suppressed the wound healing and invasion ability, and decreased the expression of Snail and Slug in T24 and 5637 cells, and matrix metalloproteinase (MMP)-9 in UMUC-3 cells. Taken together, this is the first study showing that BA suppresses the proliferation of human bladder cancer cells, which is due to induction of apoptosis, necrosis, and cell cycle arrest, and decrease of migration and invasion. Furthermore, BA-induced apoptosis is regulated by caspase-dependent and ROS-independent pathways, and these results provide the underlying anti-proliferative molecular mechanism of BA in human bladder cancer cells.

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