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

J 2014

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

HORAK, Peter; Erwin TOMASICH; Petr VAŇHARA; Kateřina KRATOCHVÍLOVÁ; Mariam ANEES et al.

Základní údaje

Originální název

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

Autoři

Vydání

Scientific Reports, London, Nature Publishing Group, 2014, 2045-2322

Další údaje

Jazyk

angličtina

Typ výsledku

Článek v odborném periodiku

Obor

30200 3.2 Clinical medicine

Stát vydavatele

Velká Británie a Severní Irsko

Utajení

není předmětem státního či obchodního tajemství

Impakt faktor

Impact factor: 5.578

Označené pro přenos do RIV

Ano

Kód RIV

RIV/00216224:14110/14:00075600

Organizační jednotka

Lékařská fakulta

Klíčová slova anglicky

POSTTRANSLATIONAL N-GLYCOSYLATION; RECESSIVE MENTAL-RETARDATION; ENDOPLASMIC-RETICULUM STRESS; UNFOLDED PROTEIN RESPONSE; XBP1 MESSENGER-RNA; CHROMOSOME ARM 8P; OVARIAN-CANCER; OLIGOSACCHARYLTRANSFERASE; DELETION; GENE

Štítky

EL OK

Příznaky

Mezinárodní význam, Recenzováno

Změněno: 2. 6. 2014 15:41, Soňa Böhmová

Anotace

V originále

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 and stress 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.

Návaznosti

7AMB12AT019, projekt VaV

Název: Studium molekulární podstaty nových tumorových markerů u ovariálních a prostatických karcinomů (Akronym: Biomarkers)

Investor: Ministerstvo školství, mládeže a tělovýchovy ČR, Studium molekulární podstaty nových tumorových markerů u ovariálních a prostatických karcinomů

Citovat

HORAK, Peter; Erwin TOMASICH; Petr VAŇHARA; Kateřina KRATOCHVÍLOVÁ; Mariam ANEES; Maximilian MARHOLD; Christof E. LEMBERGER; Marion GERSCHPACHER; Reinhard HORVAT; Maria SIBILIA; Dietmar PILS a Michael KRAINER. TUSC3 Loss Alters the ER Stress Response and Accelerates Prostate Cancer Growth in vivo. Scientific Reports. London: Nature Publishing Group, 2014, roč. 4, "3739", s. 1-9. ISSN 2045-2322. Dostupné z: https://doi.org/10.1038/srep03739.

@article{1184606,
   author = {Horak, Peter and Tomasich, Erwin and Vaňhara, Petr and Kratochvílová, Kateřina and Anees, Mariam and Marhold, Maximilian and Lemberger, Christof E. and Gerschpacher, Marion and Horvat, Reinhard and Sibilia, Maria and Pils, Dietmar and Krainer, Michael},
   article_location = {London},
   article_number = {"3739"},
   doi = {https://doi.org/10.1038/srep03739},
   keywords = {POSTTRANSLATIONAL N-GLYCOSYLATION; RECESSIVE MENTAL-RETARDATION; ENDOPLASMIC-RETICULUM STRESS; UNFOLDED PROTEIN RESPONSE; XBP1 MESSENGER-RNA; CHROMOSOME ARM 8P; OVARIAN-CANCER; OLIGOSACCHARYLTRANSFERASE; DELETION; GENE},
   language = {eng},
   issn = {2045-2322},
   journal = {Scientific Reports},
   title = {TUSC3 Loss Alters the ER Stress Response and Accelerates Prostate Cancer Growth in vivo},
   volume = {4},
   year = {2014}
}

TY  - JOUR
ID  - 1184606
AU  - Horak, Peter - Tomasich, Erwin - Vaňhara, Petr - Kratochvílová, Kateřina - Anees, Mariam - Marhold, Maximilian - Lemberger, Christof E. - Gerschpacher, Marion - Horvat, Reinhard - Sibilia, Maria - Pils, Dietmar - Krainer, Michael
PY  - 2014
TI  - TUSC3 Loss Alters the ER Stress Response and Accelerates Prostate Cancer Growth in vivo
JF  - Scientific Reports
VL  - 4
IS  - "3739"
SP  - 1-9
EP  - 1-9
PB  - Nature Publishing Group
SN  - 20452322
KW  - POSTTRANSLATIONAL N-GLYCOSYLATION
KW  - RECESSIVE MENTAL-RETARDATION
KW  - ENDOPLASMIC-RETICULUM STRESS
KW  - UNFOLDED PROTEIN RESPONSE
KW  - XBP1 MESSENGER-RNA
KW  - CHROMOSOME ARM 8P
KW  - OVARIAN-CANCER
KW  - OLIGOSACCHARYLTRANSFERASE
KW  - DELETION
KW  - GENE
N2  - 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 and stress 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.
ER  -

HORAK, Peter; Erwin TOMASICH; Petr VAŇHARA; Kateřina KRATOCHVÍLOVÁ; Mariam ANEES; Maximilian MARHOLD; Christof E. LEMBERGER; Marion GERSCHPACHER; Reinhard HORVAT; Maria SIBILIA; Dietmar PILS a Michael KRAINER. TUSC3 Loss Alters the ER Stress Response and Accelerates Prostate Cancer Growth in vivo. \textit{Scientific Reports}. London: Nature Publishing Group, 2014, roč.~4, ''3739'', s.~1-9. ISSN~2045-2322. Dostupné z: https://doi.org/10.1038/srep03739.

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