NDLI: Inhibition of epithelial-mesenchymal transition in bladder cancer cells via modulation of mTOR signalling

Content Provider	Springer Nature Link
Author	Iskender, Banu Izgi, Kenan Hizar, Esra Jauch, Johann Arslanhan, Aslihan Yuksek, Esra Hilal Canatan, Halit
Copyright Year	2015
Abstract	Mounting evidence suggests that signalling cross-talk plays a significant role in the regulation of epithelial–mesenchymal transition (EMT) in cancer cells. However, the complex network regulating the EMT in different cancer types has not been fully described yet which affects the development of novel therapeutic strategies. In the present study, we investigated the signalling pathways involved in EMT of bladder cancer cells and demonstrated the effects of two novel agents in the regulation of EMT. Myrtucommulone-A (MC-A) and thymoquinone (TQ) have been shown to possess anti-cancer properties. However, their targets in the regulation of cancer cell behavior are not well defined. Here, we defined the effects of two putative anti-cancer agents on bladder cancer cell migration and their possible intracellular targets in the regulation of EMT. Our results suggest that MC-A or TQ treatment affected N-cadherin, Snail, Slug, and β-catenin expressions and effectively attenuated mTOR activity. The downstream components in mTOR signalling were also affected. MC-A treatment resulted in the concomitant inhibition of extracellular matrix-regulated protein kinases 1 and 2 (ERK 1/2), p38 mitogen-activated protein kinase (MAPK) and Src activity. On the other hand, TQ treatment increased Src activity while exerting no effect on ERK 1/2 or p38 MAPK activity. Given the stronger inhibition of EMT-related markers in MC-A-treated samples, we concluded that this effect might be due to collective inhibition of multiple signalling pathways which result in a decrease in their cross-talk in bladder cancer cells. Overall, the data in this study proposes novel action mechanisms for MC-A or TQ in bladder cancer cells and highlights the potential use of these active compounds in the regulation of EMT.
Starting Page	8281
Ending Page	8291
Page Count	11
File Format	PDF
ISSN	10104283
Journal	Tumor Biology
Volume Number	37
Issue Number	6
e-ISSN	14230380
Language	English
Publisher	Springer Netherlands
Publisher Date	2015-12-30
Publisher Place	Dordrecht
Access Restriction	Subscribed
Subject Keyword	Bladder cancer T24 Epithelial–mesenchymal transition mTOR Rapamycin Myrtucommulone-A Thymoquinone Cancer Research
Content Type	Text
Resource Type	Article
Subject	Medicine Cancer Research

Sl.	Authority	Responsibilities	Communication Details
1	Ministry of Education (GoI), Department of Higher Education	Sanctioning Authority	https://www.education.gov.in/ict-initiatives
2	Indian Institute of Technology Kharagpur	Host Institute of the Project: The host institute of the project is responsible for providing infrastructure support and hosting the project	https://www.iitkgp.ac.in
3	National Digital Library of India Office, Indian Institute of Technology Kharagpur	The administrative and infrastructural headquarters of the project	Dr. B. Sutradhar bsutra@ndl.gov.in
4	Project PI / Joint PI	Principal Investigator and Joint Principal Investigators of the project	Dr. B. Sutradhar bsutra@ndl.gov.in Prof. Saswat Chakrabarti will be added soon
5	Website/Portal (Helpdesk)	Queries regarding NDLI and its services	support@ndl.gov.in
6	Contents and Copyright Issues	Queries related to content curation and copyright issues	content@ndl.gov.in
7	National Digital Library of India Club (NDLI Club)	Queries related to NDLI Club formation, support, user awareness program, seminar/symposium, collaboration, social media, promotion, and outreach	clubsupport@ndl.gov.in
8	Digital Preservation Centre (DPC)	Assistance with digitizing and archiving copyright-free printed books	dpc@ndl.gov.in
9	IDR Setup or Support	Queries related to establishment and support of Institutional Digital Repository (IDR) and IDR workshops	idr@ndl.gov.in

Inhibition of epithelial-mesenchymal transition in bladder cancer cells via modulation of mTOR signalling.

Novel anti-cancer agent myrtucommulone-A and thymoquinone abrogate epithelial–mesenchymal transition in cancer cells mainly through the inhibition of PI3K/AKT signalling axis

Evaluation of transforming growth factor-β1 suppress Pokemon/epithelial–mesenchymal transition expression in human bladder cancer cells

NANOG regulates epithelial-mesenchymal transition via AMPK/mTOR signalling pathway in ovarian cancer SKOV-3 and A2780 cells.

Priming hMSCs with a putative anti-cancer compound, myrtucommulone-a: a way to harness hMSC cytokine expression via modulating PI3K/Akt pathway?

TGF-β1 regulates invasion and migration of human bladder cancer cells T24 through epithelial mesenchymal transition

NOV is upregulated and promotes migration and invasion in bladder cancer

Twisted Epithelial-to-Mesenchymal Transition Promotes Progression of Surviving Bladder Cancer T24 Cells with hTERT-Dysfunction

1-Methyl-D-Tryptophan Potentiates TGF-β-Induced Epithelial-Mesenchymal Transition in T24 Human Bladder Cancer Cells

Inhibition of epithelial-mesenchymal transition in bladder cancer cells via modulation of mTOR signalling

Similar Documents

Inhibition of epithelial-mesenchymal transition in bladder cancer cells via modulation of mTOR signalling.

Novel anti-cancer agent myrtucommulone-A and thymoquinone abrogate epithelial–mesenchymal transition in cancer cells mainly through the inhibition of PI3K/AKT signalling axis

Evaluation of transforming growth factor-β1 suppress Pokemon/epithelial–mesenchymal transition expression in human bladder cancer cells

NANOG regulates epithelial-mesenchymal transition via AMPK/mTOR signalling pathway in ovarian cancer SKOV-3 and A2780 cells.

Priming hMSCs with a putative anti-cancer compound, myrtucommulone-a: a way to harness hMSC cytokine expression via modulating PI3K/Akt pathway?

TGF-β1 regulates invasion and migration of human bladder cancer cells T24 through epithelial mesenchymal transition

NOV is upregulated and promotes migration and invasion in bladder cancer

Twisted Epithelial-to-Mesenchymal Transition Promotes Progression of Surviving Bladder Cancer T24 Cells with hTERT-Dysfunction

1-Methyl-D-Tryptophan Potentiates TGF-β-Induced Epithelial-Mesenchymal Transition in T24 Human Bladder Cancer Cells

Inhibition of epithelial-mesenchymal transition in bladder cancer cells via modulation of mTOR signalling