ArticleThe American journal of pathology2014
Prostate epithelium-specific deletion of the selenocysteine tRNA gene Trsp leads to early onset intraepithelial neoplasia.
Article in The American journal of pathology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 18 citations in OpenAlex.
- Selenium compounds for cancer prevention and therapy - human clinical trial considerations.Medical review (2021) · 2025Review
- Selenium in Prostate Cancer: Prevention, Progression, and Treatment.Pharmaceuticals (Basel, Switzerland) · 2023Review
- tRNA Function and Dysregulation in Cancer.Frontiers in cell and developmental biology · 2022Review
- Historical Roles of Selenium and Selenoproteins in Health and Development: The Good, the Bad and the Ugly.International journal of molecular sciences · 2021Review
- Role of Selenoproteins in Redox Regulation of Signaling and the Antioxidant System: A Review.Antioxidants (Basel, Switzerland) · 2020Review
- Selenoproteins of the Human Prostate: Unusual Properties and Role in Cancer Etiology.Biological trace element research · 2019Review
- Oxidative stress and prostatic diseases.Molecular and clinical oncology · 2017Article
- Selenoproteins in Tumorigenesis and Cancer Progression.Advances in cancer research · 2017Review
- Selenoprotein H is an essential regulator of redox homeostasis that cooperates with p53 in development and tumorigenesis.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
- Paradoxical Roles of Antioxidant Enzymes: Basic Mechanisms and Health Implications.Physiological reviews · 2016Review
- Cancer chemoprevention research with selenium in the post-SELECT era: Promises and challenges.Nutrition and cancer · 2016Review
- Selenium and selenocysteine: roles in cancer, health, and development.Trends in biochemical sciences · 2014Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Although various lines of evidence suggest that oxidative stress plays a role in human prostate cancer initiation and progression, there is a paucity of direct evidence for its role in tumor initiation. To begin to address this issue, we developed a novel tumorigenesis model by reducing the expression of multiple selenoproteins (SPs) in mouse prostatic epithelium. This was accomplished via the prostate-specific deletion of Trsp, a gene that encodes a transfer RNA (Sec tRNA) required for the insertion of selenocysteine residues into SPs during their translation. By 6 weeks of age, Trsp-deficient mice exhibited widespread prostatic intraepithelial neoplasia lesions in all prostatic lobes, which then progressed to high-grade dysplasia and microinvasive carcinoma by 24 weeks. In contrast to other murine prostate cancer models, Trsp-deficient mice required neither the deletion of a tumor suppressor nor the transgenic introduction of an oncogene for prostatic intraepithelial neoplasia lesion development. In keeping with the antioxidant functions of several SPs, we found increases in lipid peroxidation markers in Trsp-deficient epithelial cells. This novel model of prostate neoplasia provides evidence for the existence of a selenoprotein or selenoproteins capable of acting as a tumor suppressor in the murine prostate.
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