Exploring the prognostic significance of set-domain containing 2 (setd2) expression in advanced and castrate-resistant prostate cancer

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dc.authorid0000-0001-6657-9738
dc.contributor.authorGamallat, Yaser
dc.contributor.authorFelipe Lima, Joema
dc.contributor.authorSeyedi, Sima
dc.contributor.authorLi, Qiaowang
dc.contributor.authorRokne, Jon George
dc.contributor.authorAlhajj, Reda
dc.contributor.authorGhosh, Sunita
dc.contributor.authorBismar, Tarek A.
dc.date.accessioned2024-05-15T06:02:45Z
dc.date.available2024-05-15T06:02:45Z
dc.date.issued2024
dc.departmentİstanbul Medipol Üniversitesi, Mühendislik ve Doğa Bilimleri Fakültesi, Bilgisayar Mühendisliği Bölümü
dc.description.abstractSET-domain containing 2 (SETD2) is a histone methyltransferase and an epigenetic modifier with oncogenic functionality. In the current study, we investigated the potential prognostic role of SETD2 in prostate cancer. A cohort of 202 patients’ samples was assembled on tissue microarrays (TMAs) containing incidental, advanced, and castrate-resistant CRPCa cases. Our data showed significant elevated SETD2 expression in advanced and castrate-resistant disease (CRPCa) compared to incidental cases (2.53 ± 0.58 and 2.21 ± 0.63 vs. 1.9 ± 0.68; p < 0.001, respectively). Interestingly, the mean intensity of SETD2 expression in deceased vs. alive patients was also significantly different (2.31 ± 0.66 vs. 2 ± 0.68; p = 0.003, respectively). Overall, high SETD2 expression was found to be considered high risk and was significantly associated with poor prognosis and worse overall survival (OS) (HR 1.80; 95% CI: 1.28–2.53, p = 0.001) and lower cause specific survival (CSS) (HR 3.14; 95% CI: 1.94–5.08, p < 0.0001). Moreover, combining high-intensity SETD2 with PTEN loss resulted in lower OS (HR 2.12; 95% CI: 1.22–3.69, p = 0.008) and unfavorable CSS (HR 3.74; 95% CI: 1.67–8.34, p = 0.001). Additionally, high SETD2 intensity with ERG positive expression showed worse prognosis for both OS (HR 1.99, 95% CI 0.87–4.59; p = 0.015) and CSS (HR 2.14, 95% CI 0.98–4.68, p = 0.058). We also investigated the protein expression database TCPA, and our results showed that high SETD2 expression is associated with a poor prognosis. Finally, we performed TCGA PRAD gene set enrichment analysis (GSEA) data for SETD2 overexpression, and our data revealed a potential association with pathways involved in tumor progression such as the AMPK signaling pathway, the cAMP signaling pathway, and the PI3K-Akt signaling pathway, which are potentially associated with tumor progression, chemoresistance, and a poor prognosis.
dc.description.sponsorshipProstate Cancer Foundation Young Investigator Awarden_US
dc.identifier.citationGamallat, Y., Felipe Lima, J., Seyedi, S., Li, Q., Rokne, J. G., Alhajj, R. ... Bismar, T. A. (2024). Exploring the prognostic significance of set-domain containing 2 (setd2) expression in advanced and castrate-resistant prostate cancer. Cancers, 16(7). http://dx.doi.org/10.3390/cancers16071436
dc.identifier.doi10.3390/cancers16071436
dc.identifier.issn2072-6694
dc.identifier.issue7
dc.identifier.pmid38611113
dc.identifier.scopus2-s2.0-85190124811
dc.identifier.scopusqualityQ1
dc.identifier.urihttp://dx.doi.org/10.3390/cancers16071436
dc.identifier.urihttps://hdl.handle.net/20.500.12511/12454
dc.identifier.volume16
dc.identifier.wos001201612700001en_US
dc.identifier.wosqualityQ2
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakScopus
dc.indekslendigikaynakPubMed
dc.institutionauthorAlhajj, Reda
dc.language.isoen
dc.relation.ispartofCancersen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanı
dc.rightsAttribution 4.0 International*
dc.rightsinfo:eu-repo/semantics/openAccess
dc.rights.urihttps://creativecommons.org/licenses/by/4.0/*
dc.subjectCause Specific Survival
dc.subjectERG
dc.subjectOverall Survival
dc.subjectProstate Cancer
dc.subjectPTEN
dc.subjectSETD2
dc.titleExploring the prognostic significance of set-domain containing 2 (setd2) expression in advanced and castrate-resistant prostate cancer
dc.typeArticle

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