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

Varování

Publikace nespadá pod Ekonomicko-správní fakultu, ale pod Lékařskou fakultu. Oficiální stránka publikace je na webu muni.cz.

Autoři	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
Rok publikování	2014
Druh	Článek v odborném periodiku
Časopis / Zdroj	Scientific Reports
Fakulta / Pracoviště MU	Lékařská fakulta
Citace
Doi	http://dx.doi.org/10.1038/srep03739
Obor	Onkologie a hematologie
Klíčová slova	POSTTRANSLATIONAL N-GLYCOSYLATION; RECESSIVE MENTAL-RETARDATION; ENDOPLASMIC-RETICULUM STRESS; UNFOLDED PROTEIN RESPONSE; XBP1 MESSENGER-RNA; CHROMOSOME ARM 8P; OVARIAN-CANCER; OLIGOSACCHARYLTRANSFERASE; DELETION; GENE
Popis	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.
Související projekty:	Studium molekulární podstaty nových tumorových markerů u ovariálních a prostatických karcinomů