ArticleCancer prevention research (Philadelphia, Pa.)2009
Methyl-selenium compounds inhibit prostate carcinogenesis in the transgenic adenocarcinoma of mouse prostate model with survival benefit.
Article in Cancer prevention research (Philadelphia, Pa.), 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers.
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Who cites it
59 citing papers in PubMed, 119 citations in OpenAlex.
- Effect of Dietary Methylseleninic Acid and Se-Methylselenocysteine on Carcinogen-Induced, Androgen-Promoted Prostate Carcinogenesis in Rats.Nutrition and cancer · 2022Trial
- Selenium compounds for cancer prevention and therapy - human clinical trial considerations.Medical review (2021) · 2025Review
- Selenium in cancer management: exploring the therapeutic potential.Frontiers in oncology · 2024Review
- Selective Impact of Selenium Compounds on Two Cytokine Storm Players.Journal of personalized medicine · 2023Article
- Selenium Induces Pancreatic Cancer Cell Death Alone and in Combination with Gemcitabine.Biomedicines · 2022Article
- Selenium as a Bioactive Micronutrient in the Human Diet and Its Cancer Chemopreventive Activity.Nutrients · 2021Review
- Toxicology and pharmacology of synthetic organoselenium compounds: an update.Archives of toxicology · 2021Review
- Selenium Compounds as Novel Potential Anticancer Agents.International journal of molecular sciences · 2021Review
- Chemopreventive and Anticancer Property of Selenoproteins in Obese Breast Cancer.Frontiers in pharmacology · 2021Review
- EGFR-IL-6 Signaling Axis Mediated the Inhibitory Effect of Methylseleninic Acid on Esophageal Squamous Cell Carcinoma.Frontiers in pharmacology · 2021Article
- Cellular and Molecular Progression of Prostate Cancer: Models for Basic and Preclinical Research.Cancers · 2020Review
- Selenoproteins of the Human Prostate: Unusual Properties and Role in Cancer Etiology.Biological trace element research · 2019Review
- Selenium supplementation suppresses immunological and serological features of lupus in B6.Sle1b mice.Autoimmunity · 2019Article
- Role of GDF15 in methylseleninic acid-mediated inhibition of cell proliferation and induction of apoptosis in prostate cancer cells.PloS one · 2019Article
- Selenium Species: Current Status and Potentials in Cancer Prevention and Therapy.International journal of molecular sciences · 2018Review
- Methylseleninic Acid Sensitizes Ovarian Cancer Cells to T-Cell Mediated Killing by Decreasing PDL1 and VEGF Levels.Frontiers in oncology · 2018Article
- Selenoproteins and oxidative stress-induced inflammatory tumorigenesis in the gut.Cellular and molecular life sciences : CMLS · 2017Review
- Selenoproteins in Tumorigenesis and Cancer Progression.Advances in cancer research · 2017Review
- Gene expression signatures associated with suppression of TRAMP prostate carcinogenesis by a kavalactone-rich Kava fraction.Molecular carcinogenesis · 2016Article
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9 authors at 2 institutions in 1 country.
Funding
Abstract
Chemoprevention of prostate cancer by second-generation selenium compounds in reference to selenomethionine holds strong promise to deal with the disease at the root. Here we used the transgenic adenocarcinoma mouse prostate (TRAMP) model to establish the efficacy of methylseleninic acid (MSeA) and methylselenocysteine (MSeC) against prostate carcinogenesis and to characterize potential mechanisms. Eight-week-old male TRAMP mice (C57B/6 background) were given a daily oral dose of water, MSeA, or MSeC at 3 mg Se/kg body weight and were euthanized at either 18 or 26 weeks of age. By 18 weeks of age, the genitourinary tract and dorsolateral prostate weights for the MSeA- and MSeC-treated groups were lower than for the control (P < 0.01). At 26 weeks, 4 of 10 control mice had genitourinary weight >2 g, and only 1 of 10 in each of the Se groups did. The efficacy was accompanied by delayed lesion progression, increased apoptosis, and decreased proliferation without appreciable changes of T-antigen expression in the dorsolateral prostate of Se-treated mice and decreased serum insulin-like growth factor I when compared with control mice. In another experiment, giving MSeA to TRAMP mice from 10 or 16 weeks of age increased their survival to 50 weeks of age, and delayed the death due to synaptophysin-positive neuroendocrine carcinomas and synaptophysin-negative prostate lesions and seminal vesicle hypertrophy. Wild-type mice receiving MSeA from 10 weeks did not exhibit decreased body weight or genitourinary weight or increased serum alanine aminotransferase compared with the control mice. Therefore, these selenium compounds may effectively inhibit this model of prostate cancer carcinogenesis.
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