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

Warning

This publication doesn't include Faculty of Arts. It includes Faculty of Medicine. Official publication website can be found on muni.cz.
Authors

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

Year of publication 2014
Type Article in Periodical
Magazine / Source Scientific Reports
MU Faculty or unit

Faculty of Medicine

Citation
Doi http://dx.doi.org/10.1038/srep03739
Field Oncology and hematology
Keywords POSTTRANSLATIONAL N-GLYCOSYLATION; RECESSIVE MENTAL-RETARDATION; ENDOPLASMIC-RETICULUM STRESS; UNFOLDED PROTEIN RESPONSE; XBP1 MESSENGER-RNA; CHROMOSOME ARM 8P; OVARIAN-CANCER; OLIGOSACCHARYLTRANSFERASE; DELETION; GENE
Description 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.
Related projects:

You are running an old browser version. We recommend updating your browser to its latest version.