TUSC3 Loss Alters the ER Stress Response and Accelerates Prostate Cancer Growth in vivo

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00216224%3A14110%2F14%3A00075600" target="_blank" >RIV/00216224:14110/14:00075600 - isvavai.cz</a>

Výsledek na webu

<a href="http://dx.doi.org/10.1038/srep03739" target="_blank" >http://dx.doi.org/10.1038/srep03739</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.1038/srep03739" target="_blank" >10.1038/srep03739</a>

Jazyk výsledku

angličtina

Název v původním jazyce

TUSC3 Loss Alters the ER Stress Response and Accelerates Prostate Cancer Growth in vivo

Popis výsledku v původním jazyce

Prostate cancer is the most prevalent cancer in males in developed countries. Tumor suppressor candidate 3 (TUSC3) has been identified as a putative tumor suppressor gene in prostate cancer, though its function has not been characterized. TUSC3 shares homologies with the yeast oligosaccharyltransferase (OST) complex subunit Ost3p, suggesting a role in protein glycosylation. We provide evidence that TUSC3 is part of the OST complex and affects N-linked glycosylation in mammalian cells. Loss of TUSC3 expression in DU145 and PC3 prostate cancer cell lines leads to increased proliferation, migration and invasion as well as accelerated xenograft growth in a PTEN negative background. TUSC3 downregulation also affects endoplasmic reticulum (ER) structure andstress response, which results in increased Akt signaling. Together, our findings provide first mechanistic insight in TUSC3 function in prostate carcinogenesis in general and N-glycosylation in particular.

Název v anglickém jazyce

TUSC3 Loss Alters the ER Stress Response and Accelerates Prostate Cancer Growth in vivo

Popis výsledku anglicky

Prostate cancer is the most prevalent cancer in males in developed countries. Tumor suppressor candidate 3 (TUSC3) has been identified as a putative tumor suppressor gene in prostate cancer, though its function has not been characterized. TUSC3 shares homologies with the yeast oligosaccharyltransferase (OST) complex subunit Ost3p, suggesting a role in protein glycosylation. We provide evidence that TUSC3 is part of the OST complex and affects N-linked glycosylation in mammalian cells. Loss of TUSC3 expression in DU145 and PC3 prostate cancer cell lines leads to increased proliferation, migration and invasion as well as accelerated xenograft growth in a PTEN negative background. TUSC3 downregulation also affects endoplasmic reticulum (ER) structure andstress response, which results in increased Akt signaling. Together, our findings provide first mechanistic insight in TUSC3 function in prostate carcinogenesis in general and N-glycosylation in particular.

Druh

J_x - Nezařazeno - Článek v odborném periodiku (Jimp, Jsc a Jost)

CEP obor

FD - Onkologie a hematologie

OECD FORD obor

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Projekt

<a href="/cs/project/7AMB12AT019" target="_blank" >7AMB12AT019: Studium molekulární podstaty nových tumorových markerů u ovariálních a prostatických karcinomů</a><br>

Návaznosti

P - Projekt vyzkumu a vyvoje financovany z verejnych zdroju (s odkazem do CEP)

Rok uplatnění

2014

Kód důvěrnosti údajů

S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Název periodika

Scientific Reports

ISSN

2045-2322

e-ISSN

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Svazek periodika

4

Číslo periodika v rámci svazku

"3739"

Stát vydavatele periodika

GB - Spojené království Velké Británie a Severního Irska

Počet stran výsledku

9

Strana od-do

1-9

Kód UT WoS článku

000329849100005

EID výsledku v databázi Scopus

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