Epigenetic silencing of the human 18 kDa translocator protein in a T cell leukemia cell line

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dc.contributor.authorMiddleton, RJen_AU
dc.contributor.authorKam, WWYen_AU
dc.contributor.authorLiu, GJen_AU
dc.contributor.authorBanati, RBen_AU
dc.date.accessioned2020-03-23T03:00:46Zen_AU
dc.date.available2020-03-23T03:00:46Zen_AU
dc.date.issued2017-02-01en_AU
dc.description.abstractThe mitochondrial membrane 18 kDa translocator protein (TSPO), previously known as the peripheral benzodiazepine receptor, is constitutively expressed in most organs, most abundantly in hormonal tissue and cells of mononuclear phagocyte lineage, while in the brain, TSPO expression is induced in the wake of injury, inflammation, and neurodegeneration. Increased TSPO expression is also prominent in several cancerous tissues where it appears to correlate with the degree of malignancy. Currently, TSPO is thus actively investigated as a generic biomarker for disease activity and a therapeutic target for a wide range of diseases. In this study, we report a Jurkat human T cell leukemia cell line that has only trace expression of TSPO mRNA. Through the use of bisulphite genomic sequencing, we show that the Jurkat TSPO promoter is highly methylated except for CpG sites that are adjacent to the transcription start site. Control measurements in HEK-293, HeLa, and U87-MG cells with high TSPO mRNA expression showed low levels of TSPO promoter methylation. Demethylation with 5-aza-2'-deoxycytidine (5-aza-dC) caused a dose-dependent increase in TSPO mRNA with a corresponding demethylation of the TSPO promoter in Jurkat cells. Treating HeLa and U87-MG cells with 5-aza-dC caused no change in the level of TSPO mRNA. These observations confirm the epigenetic regulation of TSPO and suggest it to be a more common mechanism by which the differential expression of TSPO in various cell types and in health and disease may be explained. ©2017 Mary Ann Liebert, Inc.en_AU
dc.identifier.citationMiddleton, R. J., Kam, W. W. Y., Liu, G. J., & Banati, R. B. (2017). Epigenetic silencing of the human 18 kDa translocator protein in a T cell leukemia cell line. DNA and Cell Biology, 36(2), 103-108. doi:10.1089/dna.2016.3385en_AU
dc.identifier.govdoc8823en_AU
dc.identifier.issn1044-5498en_AU
dc.identifier.issue2en_AU
dc.identifier.journaltitleDNA and Cell Biologyen_AU
dc.identifier.pagination103-108en_AU
dc.identifier.urihttps://doi.org/10.1089/dna.2016.3385en_AU
dc.identifier.urihttp://apo.ansto.gov.au/dspace/handle/10238/9188en_AU
dc.identifier.volume36en_AU
dc.language.isoenen_AU
dc.publisherMary Ann Liebert, Inc. publishersen_AU
dc.subjectMethylationen_AU
dc.subjectLeukemiaen_AU
dc.subjectProteinsen_AU
dc.subjectMitochondriaen_AU
dc.subjectReceptorsen_AU
dc.subjectBiochemistryen_AU
dc.titleEpigenetic silencing of the human 18 kDa translocator protein in a T cell leukemia cell lineen_AU
dc.typeJournal Articleen_AU
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