Please use this identifier to cite or link to this item: https://ahro.austin.org.au/austinjspui/handle/1/18484
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dc.contributor.authorCheung, Ada S-
dc.contributor.authorde Rooy, Casey-
dc.contributor.authorLevinger, Itamar-
dc.contributor.authorRana, Kesha-
dc.contributor.authorClarke, Michele V-
dc.contributor.authorHow, Jackie M Y-
dc.contributor.authorGarnham, Andrew-
dc.contributor.authorMcLean, Catriona-
dc.contributor.authorZajac, Jeffrey D-
dc.contributor.authorDavey, Rachel A-
dc.contributor.authorGrossmann, Mathis-
dc.date2017-07-27-
dc.date.accessioned2018-08-30T06:06:19Z-
dc.date.available2018-08-30T06:06:19Z-
dc.date.issued2017-11-
dc.identifier.citationThe Journal of Steroid Biochemistry and Molecular Biology 2017; 174: 56-64en_US
dc.identifier.urihttps://ahro.austin.org.au/austinjspui/handle/1/18484-
dc.description.abstractAndrogen deprivation therapy (ADT) decreases muscle mass and function but no human studies have investigated the underlying genetic or cellular effects. We tested the hypothesis that ADT will lead to changes in skeletal muscle gene expression, which may explain the adverse muscle phenotype seen clinically. We conducted a prospective cohort study of 9 men with localised prostate cancer who underwent a vastus lateralis biopsy before and after 4 weeks of ADT. Next-generation RNA sequencing was performed and genes differentially expressed following ADT underwent gene ontology mining using Ingenuity Pathway Analysis. Differential expression of genes of interest was confirmed by quantitative PCR (Q-PCR) on gastrocnemius muscle of orchidectomised mice and sham controls (n=11/group). We found that in men, circulating total testosterone decreased from 16.5±4.3nmol/L at baseline to 0.4±0.15nmol/L post-ADT (p<0.001). RNA sequencing identified 19 differentially expressed genes post-ADT (all p<0.05 after adjusting for multiple testing). Gene ontology mining identified 8 genes to be of particular interest due to known roles in androgen-mediated signalling; ABCG1, ACTC1, ANKRD1, DMPK, THY1, DCLK1, CST3 were upregulated and SLC38A3 was downregulated post-ADT. Q-PCR in mouse gastrocnemius muscle confirmed that only one gene, Actc1 was concordantly upregulated (p<0.01) in orchidectomised mice compared with controls. In conclusion, given that ACTC1 upregulation is associated with improved muscle function in certain myopathies, we hypothesise that upregulation of ACTC1 may represent a compensatory response to ADT-induced muscle loss. Further studies will be required to evaluate the role and function of ACTC1.en_US
dc.language.isoeng-
dc.subjectAndrogensen_US
dc.subjectGeneen_US
dc.subjectMuscleen_US
dc.subjectProstatic neoplasmsen_US
dc.titleActin alpha cardiac muscle 1 gene expression is upregulated in the skeletal muscle of men undergoing androgen deprivation therapy for prostate cancer.en_US
dc.typeJournal Articleen_US
dc.identifier.journaltitleThe Journal of Steroid Biochemistry and Molecular Biologyen_US
dc.identifier.affiliationDepartment of Pathology, Alfred Health, Victoria, Australiaen_US
dc.identifier.affiliationEndocrinologyen_US
dc.identifier.affiliationMedicine (University of Melbourne)en_US
dc.identifier.affiliationInstitute of Sport, Exercise, and Active Living (ISEAL), Victoria University, Victoria, Australiaen_US
dc.identifier.affiliationAustralian Institute for Musculoskeletal Science (AIMSS), Western Health, St. Albans, Victoria, Australiaen_US
dc.identifier.affiliationCentre for Physical Activity and Nutrition, School of Exercise and Nutrition Sciences, Deakin University, Burwood, Victoria, Australiaen_US
dc.identifier.doi10.1016/j.jsbmb.2017.07.029en_US
dc.type.contentTexten_US
dc.identifier.orcid0000-0001-5257-5525en_US
dc.identifier.orcid0000-0001-5121-0209en_US
dc.identifier.orcid0000-0001-8261-3457en_US
dc.identifier.pubmedid28756295-
dc.type.austinJournal Article-
dc.type.austinResearch Support, Non-U.S. Gov't-
local.name.researcherCheung, Ada S
item.fulltextNo Fulltext-
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.cerifentitytypePublications-
item.languageiso639-1en-
item.grantfulltextnone-
item.openairetypeJournal Article-
crisitem.author.deptEndocrinology-
crisitem.author.deptMedicine (University of Melbourne)-
crisitem.author.deptCardiology-
crisitem.author.deptEndocrinology-
crisitem.author.deptMedicine (University of Melbourne)-
crisitem.author.deptEndocrinology-
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