Please use this identifier to cite or link to this item: http://localhost:80/xmlui/handle/123456789/16520
Title: Prostate cancer: Leading and misleading routes to TRAIL of death
Authors: Farooq, Ammad Ahmad
Qureshi, Muhammad Zahid
Abdur Rehman
Nogueira, Daniele Rubert
Awan, Imrana Iftikhar
Adeela Shahid
Keywords: TRAIL, apoptosis
targeted therapy
signaling cascades
Issue Date: 20-Sep-2014
Publisher: Karachi:Pakistan Journal of Pharmaceutical Sciences, university of Karachi.
Citation: Ammad, F., Muhammad, Q., Abdur, R., Daniele, N., Imrana, A., & Adeela, S. (2014). Prostate cancer: Leading and misleading routes to TRAIL of death.
Abstract: Prostate cancer is a multifaceted disease that arises because of misrepresentation of linear and integrated signaling cascades that regulate gene network in normal and cancer cells. Programmed cell death is modulated by intracellular regulators within each cell and various lines of evidence suggest that there is under- expression and overexpression of pro-apoptotic and anti-apoptotic gene subsets respectively. Apoptosis is a response to the cellular microenvironment, and the cell microenvironment can be regulated by multiple signaling cascades at a higher organizational level by suppressing survival signals notably at genetic, epigenetic, transcriptional and post-transcriptional level. Unquestionably, drug-discovery approaches over the last decade aiming at neutralizing anti-apoptotic proteins, over-expressing pro-apoptotic proteins and enhancing the cell surface appearance of TRAIL receptors have revolutionized our current information about inducing and maximizing TRAIL mediated signaling in resistant prostate cancer phenotype. In this mini-review we outline outstanding developments in the field of prostate cancer that have played a rolein understanding the underlying mechanisms that control TRAIL mediated apoptosis in prostate cancer cells, which may be helpful in the development of cancer therapies based on the apoptotic pathway
URI: http://142.54.178.187:9060/xmlui/handle/123456789/16520
ISSN: 1011-601X
Appears in Collections:Issue 03

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