Can THEM6 targeting stop resistance to prostate cancer treatment?

Prostate cancer (PCa) clinical management relies heavily on androgen‐deprivation therapy (ADT). However, despite experiencing initial clinical benefit, patients getting ADT for non‐resectable PCa eventually relapse and develop fatal castration‐resistant PCa (CRPC). Multiple mechanisms of acquired re...

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Main Authors: Mrittika Chattopadhyay, Doris Germain
Format: Article
Language:English
Published: Springer Nature 2022-03-01
Series:EMBO Molecular Medicine
Online Access:https://doi.org/10.15252/emmm.202115504
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author Mrittika Chattopadhyay
Doris Germain
author_facet Mrittika Chattopadhyay
Doris Germain
author_sort Mrittika Chattopadhyay
collection DOAJ
description Prostate cancer (PCa) clinical management relies heavily on androgen‐deprivation therapy (ADT). However, despite experiencing initial clinical benefit, patients getting ADT for non‐resectable PCa eventually relapse and develop fatal castration‐resistant PCa (CRPC). Multiple mechanisms of acquired resistance to treatment have been reported, including metabolic adaptation (Marine et al, 2020). Notably, activation of the endoplasmic reticulum (ER) unfolded protein response (UPR) has been associated with oncogenic transformation (Hart et al, 2012), tumor progression, metastasis dissemination, and resistance to therapy (Chen & Cubillos‐Ruiz, 2021). Targeting different branches of ER UPR has been found to be an effective tool against aggressive PCa (Nguyen et al, 2018; Sheng et al, 2019). Therefore, a better understanding of these pathways may lead to the identification of novel drug targets.
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spelling doaj.art-f13114d0fdfd4579ae503e0eb5d820232024-03-02T20:52:36ZengSpringer NatureEMBO Molecular Medicine1757-46761757-46842022-03-01143n/an/a10.15252/emmm.202115504Can THEM6 targeting stop resistance to prostate cancer treatment?Mrittika Chattopadhyay0Doris Germain1Tish Cancer Institute Division of Hematology/Oncology Icahn School of Medicine at Mount Sinai New York NY USATish Cancer Institute Division of Hematology/Oncology Icahn School of Medicine at Mount Sinai New York NY USAProstate cancer (PCa) clinical management relies heavily on androgen‐deprivation therapy (ADT). However, despite experiencing initial clinical benefit, patients getting ADT for non‐resectable PCa eventually relapse and develop fatal castration‐resistant PCa (CRPC). Multiple mechanisms of acquired resistance to treatment have been reported, including metabolic adaptation (Marine et al, 2020). Notably, activation of the endoplasmic reticulum (ER) unfolded protein response (UPR) has been associated with oncogenic transformation (Hart et al, 2012), tumor progression, metastasis dissemination, and resistance to therapy (Chen & Cubillos‐Ruiz, 2021). Targeting different branches of ER UPR has been found to be an effective tool against aggressive PCa (Nguyen et al, 2018; Sheng et al, 2019). Therefore, a better understanding of these pathways may lead to the identification of novel drug targets.https://doi.org/10.15252/emmm.202115504
spellingShingle Mrittika Chattopadhyay
Doris Germain
Can THEM6 targeting stop resistance to prostate cancer treatment?
EMBO Molecular Medicine
title Can THEM6 targeting stop resistance to prostate cancer treatment?
title_full Can THEM6 targeting stop resistance to prostate cancer treatment?
title_fullStr Can THEM6 targeting stop resistance to prostate cancer treatment?
title_full_unstemmed Can THEM6 targeting stop resistance to prostate cancer treatment?
title_short Can THEM6 targeting stop resistance to prostate cancer treatment?
title_sort can them6 targeting stop resistance to prostate cancer treatment
url https://doi.org/10.15252/emmm.202115504
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