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Estrogens down-regulate the stem cell factor (SCF)/c-KIT system in prostate cells: Evidence of antiproliferative and proapoptotic effects

2016-01-01Journal article Restricted access
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dc.contributor.authorFigueira, Marília I
dc.contributor.authorCorreia, Sara
dc.contributor.authorVaz, Cátia
dc.contributor.authorCardoso, HJ
dc.contributor.authorGomes, Inês
dc.contributor.authorMarques, Ricardo
dc.contributor.authorBaptista, Cláudio
dc.contributor.authorSocorro, Sílvia
dc.date.accessioned2019-12-20T11:59:38Z
dc.date.available2019-12-20T11:59:38Z
dc.date.issued2016-01-01
dc.description.abstractThe development of prostate cancer (PCa) is intimately associated with the hormonal environment, and the sex steroids estrogens have been implicated in prostate malignancy. However, if some studies identified estrogens as causative agents of PCa, others indicated that these steroids have a protective role counteracting prostate overgrowth. The tyrosine kinase receptor c-KIT and its ligand, the stem cell factor (SCF), have been associated with the control of cell proliferation/apoptosis and prostate carcinogenesis, and studies show that estrogens regulate their expression in different tissues, though, in the case of prostate this remains unknown. The present study aims to evaluate the role of 17β-estradiol (E2) in regulating the expression of SCF/c-KIT in human prostate cell lines and rat prostate, and to investigate the consequent effects on prostate cell proliferation and apoptosis. qPCR, Western Blot, and immuno(cito)histochemistry analysis showed that E2-treatment decreased the expression of SCF and c-KIT both in human prostate cells and rat prostate. Furthermore, the diminished expression of SCF/c-KIT was underpinned by the diminished prostate weight and reduced proliferation index. On the other hand, the results of TUNEL labelling, the increased activity of caspase-3, and the augmented expression of caspase-8 and Fas system in the prostate of E2-treated animals indicated augmented apoptosis in response to E2. The obtained results demonstrated that E2 down-regulated the expression of SCF/c-KIT system in prostate cells, which was associated with antiproliferative and proapoptotic effects. Moreover, these findings support the protective role of estrogens in PCa and open new perspectives on the application of estrogen-based therapies.pt_PT
dc.description.versioninfo:eu-repo/semantics/publishedVersionpt_PT
dc.identifier.doi10.1016/j.bcp.2015.11.016pt_PT
dc.identifier.urihttp://hdl.handle.net/10400.6/7999
dc.language.isoengpt_PT
dc.peerreviewedyespt_PT
dc.relationEstrogens and prostate cancer: role of GPER and regulation of stem cell factor SCF/c-KIT system
dc.relationEffect of endocrine disruptors on spermatogenesis and testicular cancer: where does the protective role of regucalcin fit in
dc.relationROLE OF REGUCALCIN IN BREAST CELLS PROLIFERATION AND TUMOR DEVELOPMENT
dc.relationAndrogens/anti-androgens and glycaemia in reprogramming metabolism of prostate cancer: targeting both androgen receptor and metabolism as a therapeutic option
dc.subjectApoptosispt_PT
dc.subjectEstrogenspt_PT
dc.subjectProliferationpt_PT
dc.subjectProstate cancerpt_PT
dc.subjectSCFpt_PT
dc.subjectC-KITpt_PT
dc.titleEstrogens down-regulate the stem cell factor (SCF)/c-KIT system in prostate cells: Evidence of antiproliferative and proapoptotic effectspt_PT
dc.typejournal article
dspace.entity.typePublication
oaire.awardTitleEstrogens and prostate cancer: role of GPER and regulation of stem cell factor SCF/c-KIT system
oaire.awardTitleEffect of endocrine disruptors on spermatogenesis and testicular cancer: where does the protective role of regucalcin fit in
oaire.awardTitleROLE OF REGUCALCIN IN BREAST CELLS PROLIFERATION AND TUMOR DEVELOPMENT
oaire.awardTitleAndrogens/anti-androgens and glycaemia in reprogramming metabolism of prostate cancer: targeting both androgen receptor and metabolism as a therapeutic option
oaire.awardURIinfo:eu-repo/grantAgreement/FCT/5876/PEst-OE%2FSAU%2FUI0709%2F2014/PT
oaire.awardURIinfo:eu-repo/grantAgreement/FCT//SFRH%2FBD%2F104671%2F2014/PT
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oaire.awardURIinfo:eu-repo/grantAgreement/FCT//SFRH%2FBD%2F70316%2F2010/PT
oaire.awardURIinfo:eu-repo/grantAgreement/FCT/POR_CENTRO/SFRH%2FBD%2F111351%2F2015/PT
oaire.awardURIinfo:eu-repo/grantAgreement/FCT/SFRH/SFRH%2FBD%2F66875%2F2009/PT
oaire.citation.endPage87pt_PT
oaire.citation.startPage73pt_PT
oaire.citation.titleBiochemical Pharmacologypt_PT
oaire.citation.volume99pt_PT
oaire.fundingStream5876
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oaire.fundingStreamSFRH
person.familyNameFigueira
person.familyNameCorreia
person.familyNameVaz
person.familyNameCardoso
person.familyNameGomes
person.familyNameMaia Baptista
person.familyNameSocorro
person.givenNameMarília
person.givenNameSara
person.givenNameCátia
person.givenNameHenrique
person.givenNameInês
person.givenNameCláudio Jorge
person.givenNameSílvia Cristina da Cruz Marques
person.identifierhttps://scholar.google.pt/citations?user=hFKOd_QAAAAJ&hl=pt-PT&oi=ao
person.identifierhttps://scholar.google.pt/citations?user=PA3L_h8AAAAJ&hl=pt-PT
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project.funder.identifierhttp://doi.org/10.13039/501100001871
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project.funder.nameFundação para a Ciência e a Tecnologia
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rcaap.embargofctCopyright cedido à editora no momento da publicação.pt_PT
rcaap.rightsclosedAccesspt_PT
rcaap.typearticlept_PT
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