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The effects of exposing cells to the SBP1 reaction products, H<jats:sub>2<\/jats:sub>O<jats:sub>2<\/jats:sub> and H<jats:sub>2<\/jats:sub>S were also assessed. In silico analyses identified potential HNF4\u03b1 binding sites within the <jats:italic>SBP1<\/jats:italic> promoter region and this was investigated using an inhibitor specific for that transcription factor.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>Using in silico analyses, it was determined that the promoter region of <jats:italic>SBP1<\/jats:italic> contains putative binding sites for the HNF4\u03b1 transcription factor. The potential for HNF4\u03b1 to regulate <jats:italic>SBP1<\/jats:italic> expression was supported by data indicating that HNF4\u03b1 inhibition resulted in a dose\u2010response increase in the levels of SBP1 messenger RNA and protein, identifying HNF4\u03b1 as a novel negative regulator of SBP1 expression in prostate cancer cells. The consequences of altering the levels of SBP1 were investigated by ectopically expressing SBP1 in PC\u20103 prostate cancer cells, where SBP1 expression attenuated anchorage\u2010independent cellular growth and migration in culture, both properties associated with transformation. SBP1 overexpression reduced oxygen consumption in these cells and increased the activation of AMP\u2010activated protein kinase (AMPK), a major regulator of energy homeostasis. In addition, the reaction products of SBP1, H<jats:sub>2<\/jats:sub>O<jats:sub>2<\/jats:sub>, and H<jats:sub>2<\/jats:sub>S also activated AMPK.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions<\/jats:title><jats:p>Based on the obtained data, it is hypothesized that SBP1 negatively regulates oxidative phosphorylation (OXPHOS) in the healthy prostate cells by the production of H<jats:sub>2<\/jats:sub>O<jats:sub>2<\/jats:sub> and H<jats:sub>2<\/jats:sub>S and consequential activation of AMPK. The reduction of SBP1 levels in prostate cancer can occur due to increased binding of HNF4\u03b1, acting as a transcriptional inhibitor to the <jats:italic>SBP1<\/jats:italic> promoter. Consequently, there is a reduction in H<jats:sub>2<\/jats:sub>O<jats:sub>2<\/jats:sub> and H<jats:sub>2<\/jats:sub>S\u2010mediated signaling, inhibition of AMPK, and stimulation of OXPHOS and building blocks of biomolecules needed for tumor growth and progression. Other effects of SBP1 loss in tumor cells remain to be discovered.<\/jats:p><\/jats:sec>","DOI":"10.1002\/pros.24028","type":"journal-article","created":{"date-parts":[[2020,6,8]],"date-time":"2020-06-08T17:54:46Z","timestamp":1591638886000},"page":"962-976","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":24,"title":["Selenium\u2010binding protein 1 alters energy metabolism in prostate cancer cells"],"prefix":"10.1002","volume":"80","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-0841-8017","authenticated-orcid":false,"given":"Mostafa","family":"Elhodaky","sequence":"first","affiliation":[{"name":"Department of Pathology, College of Medicine University of Illinois at Chicago Chicago Illinois"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lenny K.","family":"Hong","sequence":"additional","affiliation":[{"name":"Department of Pathology, College of Medicine University of Illinois at Chicago Chicago 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