Analysis of tumor necrosis factor ?-induced and nuclear factor ?B-silenced LNCap prostate cancer cells by RT-qPCR

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dc.contributor.authorGonen-Korkmaz C.
dc.contributor.authorSevin G.
dc.contributor.authorGokce G.
dc.contributor.authorArun M.Z.
dc.contributor.authorYildirim G.
dc.contributor.authorReel B.
dc.contributor.authorKaymak A.
dc.contributor.authorOgut D.
dc.date.accessioned2019-10-27T08:22:08Z
dc.date.available2019-10-27T08:22:08Z
dc.date.issued2014
dc.departmentEge Üniversitesien_US
dc.description.abstractProstate cancer is the second leading cause of morbidity and mortality in males in the Western world. In the present study, LNCaP, which is an androgen receptor-positive and androgen-responsive prostate cancer cell line derived from lymph node metastasis, and DU145, which is an androgen receptor-negative prostate cancer cell line derived from brain metastasis, were investigated. TNF? treatment decreased p105 and p50 expression and R1881 treatment slightly decreased p105 expression but increased p50 expression with or without TNF? induction. As an aggressive prostate cancer cell line, DU145 transfected with six transmembrane protein of prostate (STAMP)1 or STAMP2 was also exposed to TNF?. Western blotting indicated that transfection with either STAMP gene caused a significant increase in NF?B expression following TNF? induction. In addition, following the treatment of LNCaP cells with TNF?, reverse transcription quantitative polymerase chain reaction (RT-qPCR) was performed with a panel of apoptosis-related gene primers. The apoptosis-related genes p53, p73, caspase 7 and caspase 9 showed statistically significant increases in expression levels while the expression levels of MDM2 and STAMP1 decreased following TNF? induction. Furthermore, LNCaP cells were transfected with a small interfering NF?B (siNF?B) construct for 1 and 4 days and induced with TNF? for the final 24 h. RT-qPCR amplifications were performed with apoptosis-related gene primers, including p53, caspases and STAMPs. However, no changes in the level of STAMP2 were observed between cells in the presence or absence of TNF? induction or between those transfected or not transfected with siNF?B; however, the level of STAMP1 was significantly decreased by TNF? induction, and significantly increased with siNF?B transfection. Silencing of the survival gene NF?B caused anti-apoptotic STAMP1 expression to increase, which repressed p53, together with MDM2. NF?B silencing had varying effects on a panel of cancer regulatory genes. Therefore, the effective inhibition of NF?B may be critical in providing a targeted pathway for prostate cancer prevention. © 2014, Spandidos Publications. All right reserved.en_US
dc.identifier.doi10.3892/etm.2014.2032
dc.identifier.endpage1700en_US
dc.identifier.issn1792-0981
dc.identifier.issn1792-0981en_US
dc.identifier.issue6en_US
dc.identifier.scopusqualityN/Aen_US
dc.identifier.startpage1695en_US
dc.identifier.urihttps://doi.org/10.3892/etm.2014.2032
dc.identifier.urihttps://hdl.handle.net/11454/26190
dc.identifier.volume8en_US
dc.indekslendigikaynakScopusen_US
dc.language.isoenen_US
dc.publisherSpandidos Publicationsen_US
dc.relation.ispartofExperimental and Therapeutic Medicineen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/openAccessen_US
dc.subjectCell cultureen_US
dc.subjectGene silencingen_US
dc.subjectNF?Ben_US
dc.subjectP53en_US
dc.subjectProstate canceren_US
dc.subjectSTAMP genesen_US
dc.subjectTNF?en_US
dc.titleAnalysis of tumor necrosis factor ?-induced and nuclear factor ?B-silenced LNCap prostate cancer cells by RT-qPCRen_US
dc.typeArticleen_US

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