Bladder cancer cell implantation in reconstructed bladder in vitro: a model of tumour recurrence

Nakamura, Kenichi; Fujiyama, Chisato; Tokuda, Yuji; Sugihara, Hajime; Masaki, Zenjiro

doi:10.1046/j.1464-4096.2001.01642.x

Cited by 9 publications

(9 citation statements)

References 11 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Organoids have previously been developed for many tissue types, ranging from colon [ 16 ] to prostate [ 17 ], and utilise tissue from many animal types, including rat, pig and human explants. Previous work in the field of bladder organoids has established spheroids [ 18 ], reliable, small scale mucosal models from rats [ 19 ] and full tissue models from porcine bladder, mostly concerned with tissue mimics for drug development [ 20 ] and disease recurrence [ 21 ] and invasion assays. To our knowledge, there are no existing studies employing bladder cancer organoids to study tissue autofluorescence dynamics, therefore ours represents the first of its kind.…”

Section: Introductionmentioning

confidence: 99%

Changes in autofluorescence based organoid model of muscle invasive urinary bladder cancer

Palmer¹,

Litvinova²,

Dunaev³

et al. 2016

Biomed. Opt. Express

View full text Add to dashboard Cite

Muscle invasive urinary bladder cancer is one of the most lethal cancers and its detection at the time of transurethral resection remains limited and diagnostic methods are urgently needed. We have developed a muscle invasive transitional cell carcinoma (TCC) model of the bladder using porcine bladder scaffold and the human bladder cancer cell line 5637. The progression of implanted cancer cells to muscle invasion can be monitored by measuring changes in the spectrum of endogenous fluorophores such as reduced nicotinamide dinucleotide (NADH) and flavins. We believe this could act as a useful tool for the study of fluorescence dynamics of developing muscle invasive bladder cancer in patients.Published by The Optical Society under the terms of the Creative Commons Attribution 4.0 License. Further distribution of this work must maintain attribution to the author(s) and the published article’s title, journal citation, and DOI.

show abstract

Section: Introductionmentioning

confidence: 99%

Changes in autofluorescence based organoid model of muscle invasive urinary bladder cancer

Palmer¹,

Litvinova²,

Dunaev³

et al. 2016

Biomed. Opt. Express

View full text Add to dashboard Cite

show abstract

“…The animal study proved that urothelial damage increased the occurrence of tumour cell implantation, but tumour cells were infrequently able to implant on normal mucosa . The urothelium appears to be an important barrier of preventing the adhesion and growth of bladder tumour cells .…”

Section: Discussionmentioning

confidence: 90%

Diabetes mellitus with poor glycemic control increases bladder cancer recurrence risk in patients with upper urinary tract urothelial carcinoma

Tai

Chen

Huang

et al. 2014

Diabetes Metabolism Res

View full text Add to dashboard Cite

show abstract

“…In this study, we applied a monolayer culture of immortalized urothelial cells (SV-HUC-1) as a model of the epithelium so that the interaction between cancer cell clusters and superficial-layer cells was not assessed. Indeed, experiments using reconstituted urothelium from porcine urinary bladders revealed that the cancer cell line would not implant on umbrella cells but would implant on the cells in the basal and intermediate layers after removing the umbrella cells [49] . Conditions of the urothelium, such as injury by operative procedures, might affect implantation.…”

Section: Discussionmentioning

confidence: 99%

Dynamic Change in p63 Protein Expression during Implantation of Urothelial Cancer Clusters

et al. 2015

View full text Add to dashboard Cite

Although the dissemination of urothelial cancer cells is supposed to be a major cause of the multicentricity of urothelial tumors, the mechanism of implantation has not been well investigated. Here, we found that cancer cell clusters from the urine of patients with urothelial cancer retain the ability to survive, grow, and adhere. By using cell lines and primary cells collected from multiple patients, we demonstrate that △ Np63α protein in cancer cell clusters was rapidly decreased through proteasomal degradation when clusters were attached to the matrix, leading to downregulation of E-cadherin and upregulation of N-cadherin. Decreased △ Np63α protein level in urothelial cancer cell clusters was involved in the clearance of the urothelium. Our data provide the first evidence that clusters of urothelial cancer cells exhibit dynamic changes in △ Np63α expression during attachment to the matrix, and decreased △ Np63α protein plays a critical role in the interaction between cancer cell clusters and the urothelium. Thus, because △ Np63α might be involved in the process of intraluminal dissemination of urothelial cancer cells, blocking the degradation of △ Np63α could be a target of therapy to prevent the dissemination of urothelial cancer.

show abstract

Bladder cancer cell implantation in reconstructed bladder in vitro: a model of tumour recurrence

Cited by 9 publications

References 11 publications

Changes in autofluorescence based organoid model of muscle invasive urinary bladder cancer

Changes in autofluorescence based organoid model of muscle invasive urinary bladder cancer

Diabetes mellitus with poor glycemic control increases bladder cancer recurrence risk in patients with upper urinary tract urothelial carcinoma

Dynamic Change in p63 Protein Expression during Implantation of Urothelial Cancer Clusters

Contact Info

Product

Resources

About