Loss of SELENOF Induces the Transformed Phenotype in Human Immortalized Prostate Epithelial Cells

SELENOF is a member of the class of selenoproteins in which the amino acid selenocysteine is co-translationally inserted into the elongating peptide in response to an in-frame UGA codon located in the 3′-untranslated (3′-UTR) region of the SELENOF mRNA. Polymorphisms in the 3′-UTR are associated wit...

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Autores principales:	Lenny K. Hong, Shrinidhi Kadkol, Maria Sverdlov, Irida Kastrati, Mostafa Elhodaky, Ryan Deaton, Karen S. Sfanos, Heidi Wang, Li Liu, Alan M. Diamond
Formato:	article
Lenguaje:	EN
Publicado:	MDPI AG 2021
Materias:	prostate cancer selenium selenoprotein tumor suppressor Biology (General) QH301-705.5 Chemistry QD1-999
Acceso en línea:	https://doaj.org/article/d78ee6b6a6ed47af8fbd28db14c010c4
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spelling	oai:doaj.org-article:d78ee6b6a6ed47af8fbd28db14c010c42021-11-11T17:26:19ZLoss of SELENOF Induces the Transformed Phenotype in Human Immortalized Prostate Epithelial Cells10.3390/ijms2221120401422-00671661-6596https://doaj.org/article/d78ee6b6a6ed47af8fbd28db14c010c42021-11-01T00:00:00Zhttps://www.mdpi.com/1422-0067/22/21/12040https://doaj.org/toc/1661-6596https://doaj.org/toc/1422-0067SELENOF is a member of the class of selenoproteins in which the amino acid selenocysteine is co-translationally inserted into the elongating peptide in response to an in-frame UGA codon located in the 3′-untranslated (3′-UTR) region of the SELENOF mRNA. Polymorphisms in the 3′-UTR are associated with an increased risk of dying from prostate cancer and these variations are functional and 10 times more frequent in the genomes of African American men. SELENOF is dramatically reduced in prostate cancer compared to benign adjacent regions. Using a prostate cancer tissue microarray, it was previously established that the reduction of SELENOF in the cancers from African American men was significantly greater than in cancers from Caucasian men. When SELENOF levels in human prostate immortalized epithelial cells were reduced with an shRNA construct, those cells acquired the ability to grow in soft agar, increased the ability to migrate in a scratch assay and acquired features of energy metabolism associated with prostate cancer. These results support a role of SELENOF loss in prostate cancer progression and further indicate that SELENOF loss and genotype may contribute to the disparity in prostate cancer mortality experienced by African American men.Lenny K. HongShrinidhi KadkolMaria SverdlovIrida KastratiMostafa ElhodakyRyan DeatonKaren S. SfanosHeidi WangLi LiuAlan M. DiamondMDPI AGarticleprostatecancerseleniumselenoproteintumor suppressorBiology (General)QH301-705.5ChemistryQD1-999ENInternational Journal of Molecular Sciences, Vol 22, Iss 12040, p 12040 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	prostate cancer selenium selenoprotein tumor suppressor Biology (General) QH301-705.5 Chemistry QD1-999
spellingShingle	prostate cancer selenium selenoprotein tumor suppressor Biology (General) QH301-705.5 Chemistry QD1-999 Lenny K. Hong Shrinidhi Kadkol Maria Sverdlov Irida Kastrati Mostafa Elhodaky Ryan Deaton Karen S. Sfanos Heidi Wang Li Liu Alan M. Diamond Loss of SELENOF Induces the Transformed Phenotype in Human Immortalized Prostate Epithelial Cells
description	SELENOF is a member of the class of selenoproteins in which the amino acid selenocysteine is co-translationally inserted into the elongating peptide in response to an in-frame UGA codon located in the 3′-untranslated (3′-UTR) region of the SELENOF mRNA. Polymorphisms in the 3′-UTR are associated with an increased risk of dying from prostate cancer and these variations are functional and 10 times more frequent in the genomes of African American men. SELENOF is dramatically reduced in prostate cancer compared to benign adjacent regions. Using a prostate cancer tissue microarray, it was previously established that the reduction of SELENOF in the cancers from African American men was significantly greater than in cancers from Caucasian men. When SELENOF levels in human prostate immortalized epithelial cells were reduced with an shRNA construct, those cells acquired the ability to grow in soft agar, increased the ability to migrate in a scratch assay and acquired features of energy metabolism associated with prostate cancer. These results support a role of SELENOF loss in prostate cancer progression and further indicate that SELENOF loss and genotype may contribute to the disparity in prostate cancer mortality experienced by African American men.
format	article
author	Lenny K. Hong Shrinidhi Kadkol Maria Sverdlov Irida Kastrati Mostafa Elhodaky Ryan Deaton Karen S. Sfanos Heidi Wang Li Liu Alan M. Diamond
author_facet	Lenny K. Hong Shrinidhi Kadkol Maria Sverdlov Irida Kastrati Mostafa Elhodaky Ryan Deaton Karen S. Sfanos Heidi Wang Li Liu Alan M. Diamond
author_sort	Lenny K. Hong
title	Loss of SELENOF Induces the Transformed Phenotype in Human Immortalized Prostate Epithelial Cells
title_short	Loss of SELENOF Induces the Transformed Phenotype in Human Immortalized Prostate Epithelial Cells
title_full	Loss of SELENOF Induces the Transformed Phenotype in Human Immortalized Prostate Epithelial Cells
title_fullStr	Loss of SELENOF Induces the Transformed Phenotype in Human Immortalized Prostate Epithelial Cells
title_full_unstemmed	Loss of SELENOF Induces the Transformed Phenotype in Human Immortalized Prostate Epithelial Cells
title_sort	loss of selenof induces the transformed phenotype in human immortalized prostate epithelial cells
publisher	MDPI AG
publishDate	2021
url	https://doaj.org/article/d78ee6b6a6ed47af8fbd28db14c010c4
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Loss of SELENOF Induces the Transformed Phenotype in Human Immortalized Prostate Epithelial Cells

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