Selenium-binding protein 1 is down-regulated in malignant melanoma
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Mandy Schott1,*, Miriam M. de Jel1,*, Julia C. Engelmann2, Philipp Renner3, Edward K. Geissler3, Anja K. Bosserhoff1 and Silke Kuphal1
1University of Erlangen, Institute of Biochemistry, Biochemistry and Molecular Medicine, Erlangen, Germany
2University of Regensburg, Institute of Functional Genomics, Statistical Bioinformatics, Regensburg, Germany
3Department of Surgery, University Medical Center Regensburg, Regensburg, Germany
Silke Kuphal, email: Silke.Kuphal@fau.de
Keywords: malignant melanoma; selenium-binding protein 1 (SELENBP1); glutathione peroxidase 1 (GPX1); Grm1 mouse model
Received: March 22, 2017 Accepted: December 28, 2017 Published: January 02, 2018
Selenium-binding protein 1 (SELENBP1) expression is reduced in various epithelial cancer entities compared to corresponding normal tissue and has already been described as a tumor suppressor involved in the regulation of cell proliferation, senescence, migration and apoptosis. We identified SELENBP1 to be down-regulated in cutaneous melanoma, a malignant cancer of pigment-producing melanocytes in the skin, which leads to the assumption that SELENBP1 also functions as tumor suppressor in the skin, as shown by others e.g. for prostate or lung carcinoma.
However, in vitro analyses indicate that SELENBP1 re-expression in human melanoma cell lines has no impact on cell proliferation, migration or tube formation of the tumor cells themselves when compared to control-transfected cells. Interestingly, supernatant taken from melanoma cell lines transfected with a SELENBP1 re-expression plasmid led to suppression of vessel formation of HMEC cells. Furthermore, SELENBP1 re-expression alters the sensitivity of melanoma cells for Vemurafenib treatment.
The data also hint to a functional interaction of SELENBP1 with GPX1 (Glutathione peroxidase 1). Low SELENBP1 mRNA levels correlate inversely with GPX1 expression in melanoma. The re-expression of SELENBP1 combined with down-regulation of GPX1 expression led to reduction of the proliferation of melanoma cells. In summary, SELENBP1 influences the tumor microenvironment and SELENBP1 action is functionally influenced by GPX1.
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