scholarly journals Modulation of G6PD affects bladder cancer via ROS accumulation and the AKT pathway in vitro

2018 ◽  
Author(s):  
Xiaoyi Chen ◽  
Zhijie Xu ◽  
Zhijian Zhu ◽  
Anqi Chen ◽  
Guanghou Fu ◽  
...  
Keyword(s):  
Bladder Cancer ◽  
Akt Pathway ◽  
Ros Accumulation

MP68-13 ESTROGEN RECEPTOR ALPHA PREVENTS BLADDER CANCER VIA INPP4B INHIBITED AKT PATHWAY IN VITRO AND IN VIVO

2015 ◽  
Vol 193 (4S) ◽  
Author(s):  
Chiuan-Ren Yeh ◽  
Iawen Hsu ◽  
Hiroshi Miyamoto ◽  
Xue-Ru Wu ◽  
Chawnshang Chang ◽  
...  
Keyword(s):  
Bladder Cancer ◽  
Estrogen Receptor ◽  
Estrogen Receptor Alpha ◽  
Akt Pathway ◽  
Receptor Alpha

scholarly journals TSPAN7 Exerts Anti-Tumor Effects in Bladder Cancer Through the PTEN/PI3K/AKT Pathway

2021 ◽  
Vol 10 ◽  
Author(s):  
Xi Yu ◽  
Shenglan Li ◽  
Mingrui Pang ◽  
Yang Du ◽  
Tao Xu ◽  
...  
Keyword(s):  
Bladder Cancer ◽  
Cell Lines ◽  
Therapeutic Potential ◽  
Tumor Grade ◽  
Biological Properties ◽  
Akt Pathway ◽  
Dynamic Regulation ◽  
Potential Marker

The tetraspanin protein superfamily participate in the dynamic regulation of cellular membrane compartments expressed in a variety of tumor types, which may alter the biological properties of cancer cells such as cell development, activation, growth and motility. The role of tetraspanin 7 (TSPAN7) has never been investigated in bladder cancer (BCa). In this study, we aimed to investigate the biological function of TSPAN7 and its therapeutic potential in human BCa. First, via reverse transcription and quantitative real-time PCR (qRT-PCR), we observed downregulation of TSPAN7 in BCa tissues samples and cell lines and found that this downregulation was associated with a relatively high tumor stage and tumor grade. Low expression of TSPAN7 was significantly correlated with a much poorer prognosis for BCa patients than was high expression. Immunohistochemistry (IHC) showed that low TSPAN7 expression was a high-risk predictor of BCa patient overall survival. Furthermore, the inhibitory effects of TSPAN7 on the proliferation and migration of BCa cell lines were detected by CCK-8, wound-healing, colony formation and transwell assays in vitro. Flow cytometry analysis revealed that TSPAN7 induced BCa cell lines apoptosis and cell cycle arrest. In vivo, tumor growth in nude mice bearing tumor xenografts could be obviously affected by overexpression of TSPAN7. Western blotting showed that overexpression of TSPAN7 activated Bax, cleaved caspase-3 and PTEN but inactivated Bcl-2, p-PI3K, and p-AKT to inhibit BCa cell growth via the PTEN/PI3K/AKT pathway. Taken together, our study will help identify a potential marker for BCa diagnosis and supply a target molecule for BCa treatment.

scholarly journals Estrogen Receptor Alpha Prevents Bladder Cancer Development via INPP4B inhibited Akt Pathway in vitro and in vivo

Oncotarget ◽  
2014 ◽  
Vol 5 (17) ◽  
pp. 7917-7935 ◽  
Author(s):  
Iawen Hsu ◽  
Chiuan-Ren Yeh ◽  
Spencer Slavin ◽  
Hiroshi Miyamoto ◽  
George J. Netto ◽  
...  
Keyword(s):  
Bladder Cancer ◽  
Estrogen Receptor ◽  
Estrogen Receptor Alpha ◽  
Cancer Development ◽  
Akt Pathway ◽  
Receptor Alpha

scholarly journals Semaphorin 4D promotes the proliferation and metastasis of bladder cancer by activating the PI3K/AKT pathway

2019 ◽  
Vol 105 (3) ◽  
pp. 231-242 ◽  
Author(s):  
Jian-jun Lu ◽  
Yao-wu Su ◽  
Chao-jun Wang ◽  
Di-feng Li ◽  
Liang Zhou
Keyword(s):  
Cell Proliferation ◽  
Bladder Cancer ◽  
Cancer Cell ◽  
Bladder Cancer Cell ◽  
Akt Pathway ◽  
Semaphorin 4D ◽  
Proliferation And Metastasis ◽  
Cell Proliferation And Metastasis

The present study aimed to investigate the role of semaphorin 4D (Sema4D) in bladder cancer cell proliferation and metastasis in vivo and in vitro. Effects of Sema4D modulation on cancer cell viability and clonogenic abilities were assessed by MTT assay and colony formation assay. Cell apoptosis, cell cycle analysis, transwell assays, and wound-healing assays were also assayed. A mouse model of bladder cancer was established to observe the tumorigenesis in vivo. Our data showed that Sema4D was 4-fold upregulated in clinical bladder cancer tissues relative to noncancerous ones and differentially expressed in bladder cancer cell lines. Knockdown of Sema4D in bladder cancer T24 and 5637 cells significantly decreased cell proliferation, clonogenic potential, and motility. On the contrary, overexpression of Sema4D in bladder cancer SV-HUC-1 cells significantly increased cell viability and motility. Concordantly, knockdown of Sema4D impaired while overexpression of Sema4D promoted bladder cancer cell growth rates in xenotransplanted mice. Cell cycle was arrested by modulation of Sema4D. Cell apoptotic rates and the mitochondrial membrane potentials were consistently increased upon knockdown of Sema4D in T24 cells and 5637 cells. Western blotting revealed that epithelial–mesenchymal transition was promoted by Sema4D. The PI3K/AKT pathway was activated upon Sema4D overexpression in SV-HUC-1 cells, while it was inactivated by knockdown of Sema4D in T24 cells. All these data suggest that Sema4D promotes cell proliferation and metastasis in bladder cancer in vivo and in vitro. The oncogenic behavior of Sema4D is achieved by activating the PI3K/AKT pathway.

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

Surface Labeling with Adhesion Protein FimH Improves Binding of Immunotherapeutic Agent Salmonella Ty21a to the Bladder Epithelium

2020 ◽  
pp. 1-12
Author(s):  
Maroeska J. Burggraaf ◽  
Lisette Waanders ◽  
Mariska Verlaan ◽  
Janneke Maaskant ◽  
Diane Houben ◽  
...  
Keyword(s):  
Bladder Cancer ◽  
Antitumor Activity ◽  
Bladder Wall ◽  
Bladder Epithelium ◽  
Modest Improvement ◽  
Adhesion Protein ◽  
Survival Experiment ◽  
Muscle Invasive

BACKGROUND: Bladder cancer is the ninth most common cancer in men. 70% of these tumors are classified as non-muscle invasive bladder cancer and those patients receive 6 intravesical instillations with Mycobacterium bovis BCG after transurethral resection. However, 30% of patients show recurrences after treatment and experience severe side effects that often lead to therapy discontinuation. Recently, another vaccine strain, Salmonella enterica typhi Ty21a, demonstrated promising antitumor activity in vivo. Here we focus on increasing bacterial retention in the bladder in order to reduce the number of instillations required and improve antitumor activity. OBJECTIVE: To increase the binding of Ty21a to the bladder wall by surface labeling of the bacteria with adhesion protein FimH and to study its effect in a bladder cancer mouse model. METHODS: Binding of Ty21a with surface-labeled FimH to the bladder wall was analyzed in vitro and in vivo. The antitumor effect of a single instillation of Ty21a+FimH in treatment was determined in a survival experiment. RESULTS: FimH-labeled Ty21a showed significant (p <  0.0001) improved binding to mouse and human cell lines in vitro. Furthermore, FimH labeled bacteria showed ∼5x more binding to the bladder than controls in vivo. Enhanced binding to the bladder via FimH labeling induced a modest improvement in median but not in overall mice survival. CONCLUSIONS: FimH labeling of Ty21a significantly improved binding to bladder tumor cells in vitro and the bladder wall in vivo. The improved binding leads to a modest increase in median survival in a single bladder cancer mouse study.

scholarly journals β-elemene alleviates airway stenosis via the ILK/Akt pathway modulated by MIR143HG sponging miR-1275

2021 ◽  
Vol 26 (1) ◽  
Author(s):  
Guoying Zhang ◽  
Cheng Xue ◽  
Yiming Zeng
Keyword(s):  
Cell Cycle ◽  
Cell Viability ◽  
Cell Model ◽  
Protective Efficacy ◽  
Rabbit Model ◽  
Akt Pathway ◽  
Loss Of Function ◽  
Airway Stenosis

Abstract Background We have previously found that β-elemene could inhibit the viability of airway granulation fibroblasts and prevent airway hyperplastic stenosis. This study aimed to elucidate the underlying mechanism and protective efficacy of β-elemene in vitro and in vivo. Methods Microarray and bioinformatic analysis were used to identify altered pathways related to cell viability in a β-elemene-treated primary cell model and to construct a β-elemene-altered ceRNA network modulating the target pathway. Loss of function and gain of function approaches were performed to examine the role of the ceRNA axis in β-elemene's regulation of the target pathway and cell viability. Additionally, in a β-elemene-treated rabbit model of airway stenosis, endoscopic and histological examinations were used to evaluate its therapeutic efficacy and further verify its mechanism of action. Results The hyperactive ILK/Akt pathway and dysregulated LncRNA-MIR143HG, which acted as a miR-1275 ceRNA to modulate ILK expression, were suppressed in β-elemene-treated airway granulation fibroblasts; β-elemene suppressed the ILK/Akt pathway via the MIR143HG/miR-1275/ILK axis. Additionally, the cell cycle and apoptotic phenotypes of granulation fibroblasts were altered, consistent with ILK/Akt pathway activity. In vivo application of β-elemene attenuated airway granulation hyperplasia and alleviated scar stricture, and histological detections suggested that β-elemene's effects on the MIR143HG/miR-1275/ILK axis and ILK/Akt pathway were in line with in vitro findings. Conclusions MIR143HG and ILK may act as ceRNA to sponge miR-1275. The MIR143HG/miR-1275/ILK axis mediates β-elemene-induced cell cycle arrest and apoptosis of airway granulation fibroblasts by modulating the ILK/Akt pathway, thereby inhibiting airway granulation proliferation and ultimately alleviating airway stenosis.

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