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Mitoribosome sensitivity to HSP70 inhibition uncovers metabolic liabilities of castration-resistant prostate cancer

ABSTRACT: TMT-MS of whole cell lysate collected from 22Rv1 castration-resistant prostate cancer cells treated with 5 µM JG-98 for 4 hours.

ORGANISM(S): Homo Sapiens (human)

SUBMITTER: Leonard M. Neckers

PROVIDER: PXD038684 | JPOST Repository | Tue Apr 25 00:00:00 BST 2023

REPOSITORIES: jPOST

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			Action	DRS
	P747-VT22-TMT10PLEX-F1.raw	Raw
	P747-VT22-TMT10PLEX-F10.raw	Raw
	P747-VT22-TMT10PLEX-F11.raw	Raw
	P747-VT22-TMT10PLEX-F12.raw	Raw
	P747-VT22-TMT10PLEX-F13.raw	Raw

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Mitoribosome sensitivity to HSP70 inhibition uncovers metabolic liabilities of castration-resistant prostate cancer.

Echtenkamp Frank J FJ Ishida Ryo R Rivera-Marquez Genesis M GM Maisiak Marisa M Johnson Oleta T OT Shrimp Jonathan H JH Sinha Arnav A Ralph Stephen John SJ Nisbet Ian I Cherukuri Murali Krishna MK Gestwicki Jason E JE Neckers Leonard M LM

PNAS nexus 20230403 4

The androgen receptor is a key regulator of prostate cancer and the principal target of current prostate cancer therapies collectively termed androgen deprivation therapies. Insensitivity to these drugs is a hallmark of progression to a terminal disease state termed castration-resistant prostate cancer. Therefore, novel therapeutic options that slow progression of castration-resistant prostate cancer and combine effectively with existing agents are in urgent need. We show that JG-98, an alloster ...[more]

PMID: 37091547

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