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The 15kDa selenoprotein and thioredoxin reductase 1 promote colon cancer by different pathways
- Source :
- PLoS ONE, Vol 10, Iss 4, p e0124487 (2015), PLoS ONE
- Publication Year :
- 2015
- Publisher :
- Public Library of Science (PLoS), 2015.
-
Abstract
- Selenoproteins mediate much of the cancer-preventive properties of the essential nutrient selenium, but some of these proteins have been shown to also have cancer-promoting effects. We examined the contributions of the 15kDa selenoprotein (Sep15) and thioredoxin reductase 1 (TR1) to cancer development. Targeted down-regulation of either gene inhibited anchorage-dependent and anchorage-independent growth and formation of experimental metastases of mouse colon carcinoma CT26 cells. Surprisingly, combined deficiency of Sep15 and TR1 reversed the anti-cancer effects observed with down-regulation of each single gene. We found that inflammation-related genes regulated by Stat-1, especially interferon-γ-regulated guanylate-binding proteins, were highly elevated in Sep15-deficient, but not in TR1-deficient cells. Interestingly, components of the Wnt/β-catenin signaling pathway were up-regulated in cells lacking both TR1 and Sep15. These results suggest that Sep15 and TR1 participate in interfering regulatory pathways in colon cancer cells. Considering the variable expression levels of Sep15 and TR1 found within the human population, our results provide insights into new roles of selenoproteins in cancer.
- Subjects :
- Thioredoxin Reductase 1
SEP15
Population
lcsh:Medicine
Biology
Mice
Cell Line, Tumor
medicine
Animals
Neoplasm Metastasis
education
Selenoproteins
lcsh:Science
Cell Proliferation
chemistry.chemical_classification
Regulation of gene expression
education.field_of_study
Mice, Inbred BALB C
Multidisciplinary
Gene Expression Profiling
lcsh:R
Wnt signaling pathway
Cancer
medicine.disease
3. Good health
chemistry
Colonic Neoplasms
Cancer research
lcsh:Q
Selenoprotein
Signal transduction
Research Article
Subjects
Details
- Language :
- English
- ISSN :
- 19326203
- Volume :
- 10
- Issue :
- 4
- Database :
- OpenAIRE
- Journal :
- PLoS ONE
- Accession number :
- edsair.doi.dedup.....ba39b54ddb67ef13c8ecbd2a9b900e1a