Unravelling disparate roles of NOTCH in bladder cancer.

Goriki, Akihiro; Seiler, Roland; Wyatt, Alexander W; Contreras-Sanz, Alberto; Bhat, Akshay; Matsubara, Akio; Hayashi, Tetsutaro; Black, Peter C (2018). Unravelling disparate roles of NOTCH in bladder cancer. Nature Reviews. Urology, 15(6), pp. 345-357. Nature Publishing Group 10.1038/s41585-018-0005-1

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The Notch pathway has been implicated in both oncogenic and tumour-suppressive roles in cancer depending on the tissue type and cellular context. However, until recently, little was known about the pathway in bladder cancer. Studies have revealed that NOTCH1 copy number and expression are decreased in bladder cancer and NOTCH1 activation in bladder cancer cell lines reduces proliferation, suggesting that NOTCH1 acts as a tumour suppressor. Furthermore, in transgenic models, bladder cancer is promoted by bladder-specific inactivation of a component of the γ-secretase complex, which liberates the intracellular domain of neurogenic locus Notch homologue protein (NOTCH) and starts the signalling cascade. By contrast, further work has demonstrated that NOTCH2 acts as an oncogene that promotes cell proliferation and metastasis through epithelial-to-mesenchymal transition, cell cycle progression, and maintenance of stemness. Studies indicating that NOTCH1 and NOTCH2 have opposite effects on the progression of bladder cancer could give rise to potential therapeutic approaches aimed at blocking or restoring the Notch pathway.

Item Type:

Journal Article (Review Article)

Division/Institute:

04 Faculty of Medicine > Department of Dermatology, Urology, Rheumatology, Nephrology, Osteoporosis (DURN) > Clinic of Urology

UniBE Contributor:

Seiler-Blarer, Roland

Subjects:

600 Technology > 610 Medicine & health

ISSN:

1759-4820

Publisher:

Nature Publishing Group

Language:

English

Submitter:

Laetitia Hayoz

Date Deposited:

04 Jul 2018 17:23

Last Modified:

02 Mar 2023 23:30

Publisher DOI:

10.1038/s41585-018-0005-1

PubMed ID:

29643502

BORIS DOI:

10.7892/boris.118244

URI:

https://boris.unibe.ch/id/eprint/118244

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