Tumor suppressor candidate 3 (TUSC3) prevents the epithelial-to-mesenchymal transition and inhibits tumor growth by modulating the endoplasmic reticulum stress response in ovarian cancer cells
Language English Country United States Media print-electronic
Document type Journal Article, Research Support, Non-U.S. Gov't
PubMed
25735931
DOI
10.1002/ijc.29502
Knihovny.cz E-resources
- Keywords
- N33, TUSC3, endoplasmic reticulum stress, epithelial-to-mesenchymal transition, ovarian cancer, tumor suppressor,
- MeSH
- Epithelial-Mesenchymal Transition genetics MeSH
- Heterografts MeSH
- Humans MeSH
- Membrane Proteins genetics MeSH
- Mice, Inbred NOD MeSH
- Mice, SCID MeSH
- Mice MeSH
- Cell Line, Tumor MeSH
- Tumor Suppressor Proteins genetics MeSH
- Ovarian Neoplasms genetics MeSH
- Endoplasmic Reticulum Stress genetics MeSH
- Genes, Tumor Suppressor physiology MeSH
- Animals MeSH
- Check Tag
- Humans MeSH
- Mice MeSH
- Female MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Names of Substances
- Membrane Proteins MeSH
- Tumor Suppressor Proteins MeSH
- TUSC3 protein, human MeSH Browser
Ovarian cancer is one of the most common malignancies in women and contributes greatly to cancer-related deaths. Tumor suppressor candidate 3 (TUSC3) is a putative tumor suppressor gene located at chromosomal region 8p22, which is often lost in epithelial cancers. Epigenetic silencing of TUSC3 has been associated with poor prognosis, and hypermethylation of its promoter provides an independent biomarker of overall and disease-free survival in ovarian cancer patients. TUSC3 is localized to the endoplasmic reticulum in an oligosaccharyl tranferase complex responsible for the N-glycosylation of proteins. However, the precise molecular role of TUSC3 in ovarian cancer remains unclear. In this study, we establish TUSC3 as a novel ovarian cancer tumor suppressor using a xenograft mouse model and demonstrate that loss of TUSC3 alters the molecular response to endoplasmic reticulum stress and induces hallmarks of the epithelial-to-mesenchymal transition in ovarian cancer cells. In summary, we have confirmed the tumor-suppressive function of TUSC3 and identified the possible mechanism driving TUSC3-deficient ovarian cancer cells toward a malignant phenotype.
Department of Biochemistry Quaid i Azam University Islamabad Pakistan
Department of Experimental Biology Faculty of Science Masaryk University Brno Czech Republic
Department of Histology and Embryology Faculty of Medicine Masaryk University Brno Czech Republic
References provided by Crossref.org
TUSC3: functional duality of a cancer gene
