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Salinomycin inhibits prostate cancer growth and migration via induction of oxidative stress
Medical Biotechnology, VTT Technical Research Centre of Finland, Espoo, Finland; University of Turku, Turku, Finland.
VTT Technical Research Centre of Finland, Espoo, Finland.
Örebro University, School of Science and Technology. VTT Technical Research Centre of Finland, Espoo, Finland.
VTT Technical Research Centre of Finland, Espoo, Finland.
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2012 (English)In: British Journal of Cancer, ISSN 0007-0920, E-ISSN 1532-1827, Vol. 106, no 1, p. 99-106Article in journal (Refereed) Published
Abstract [en]

BACKGROUND: We have shown that a sodium ionophore monensin inhibits prostate cancer cell growth. A structurally related compound to monensin, salinomycin, was recently identified as a putative cancer stem cell inhibitor.

METHODS: The growth inhibitory potential of salinomycin was studied in a panel of prostate cells. To get insights into the mechanism of action, a variety of assays such as gene expression and steroid profiling were performed in salinomycin-exposed prostate cancer cells.

RESULTS: Salinomycin inhibited the growth of prostate cancer cells, but did not affect non-malignant prostate epithelial cells. Salinomycin impacted on prostate cancer stem cell functions as evidenced by reduced aldehyde dehydrogenase activity and the fraction of CD44(+) cells. Moreover, salinomycin reduced the expression of MYC, AR and ERG, induced oxidative stress as well as inhibited nuclear factor-κB activity and cell migration. Furthermore, profiling steroid metabolites revealed increased levels of oxidative stress-inducing steroids 7-ketocholesterol and aldosterone and decreased levels of antioxidative steroids progesterone and pregnenolone in salinomycin-exposed prostate cancer cells.

CONCLUSION: Our results indicate that salinomycin inhibits prostate cancer cell growth and migration by reducing the expression of key prostate cancer oncogenes, inducing oxidative stress, decreasing the antioxidative capacity and cancer stem cell fraction.

Place, publisher, year, edition, pages
Nature Publishing Group, 2012. Vol. 106, no 1, p. 99-106
National Category
Cancer and Oncology Cell and Molecular Biology
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URN: urn:nbn:se:oru:diva-63661DOI: 10.1038/bjc.2011.530ISI: 000299168300015PubMedID: 22215106Scopus ID: 2-s2.0-84855396578OAI: oai:DiVA.org:oru-63661DiVA, id: diva2:1169224
Available from: 2017-12-22 Created: 2017-12-22 Last updated: 2018-05-15Bibliographically approved

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Hyötyläinen, TuuliaOresic, Matej

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