Decreased Expression of HN1 Sensitizes Prostate Cancer Cells to Apoptosis Induced by Docetaxel and 2-Methoxyestradiol

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dc.contributor.authorVarisli, Lokman
dc.date.accessioned2024-04-24T17:33:27Z
dc.date.available2024-04-24T17:33:27Z
dc.date.issued2022
dc.departmentDicle Üniversitesien_US
dc.description.abstractObjective. Prostate cancer is one of the most frequently diagnosed cancer in men and ranks as the second most common cause of cancer-related deaths in developed countries. HN1 is a highly expressed gene in prostate cancer and controls the levels of several cell cycle regulatory proteins including Cyclin B1. Cyclin B1 is a cell cycle control protein but is also involved in Docetaxel and 2-Methoxyestradiol induced apoptosis. Since Cyclin B1 level may affect chemotherapy success and HN1-Cyclin B1 negative correlation has already been shown, so in this study, we investigated the possible role of HN1 in chemotherapeutic resistance in prostate cancer cells. Methods. Androgen-dependent and independent prostate cancer cells were used in the study. A full-length human HN1 cDNA fragment was cloned to a mammalian expression vector and this construct was used for overexpression experiments. A siRNA that specifically targets HN1 was used for HN1 depletion experiments. Evaluation of apoptosis was performed by the level of PARP cleavage and an apoptosis kit that measure Caspase 3 activity. Results. The HN1 protein level is decreased in the Docetaxel or 2-Methoxyestradiol treated LNCaP and PC-3 PCa cells whereas the Cyclin B1 level is increased. HN1 overexpression inhibited Docetaxel and 2-Methoxyestradiol induced apoptosis. In concordance, its depletion further stimulated apoptosis in drug-treated cells. However, silencing of Cyclin B1 along with HN1 abolished the increased apoptotic response induced by silencing of HN1 in Docetaxel or 2-Methoxyestradiol treated cells. Conclusion. HN1 is an anti-apoptotic molecule and inhibits Docetaxel and 2-Methoxyestradiol induced apoptosis by targeting Cyclin B1.en_US
dc.description.sponsorshipScienti fic and Technological Research Council of Turkey (TUBITAK) [113S290]en_US
dc.description.sponsorshipThe author thanks the Scienti fic and Technological Research Council of Turkey (TUBITAK) for the support of this study (Grant No: 113S290) .en_US
dc.identifier.endpage201en_US
dc.identifier.issn0091-7370
dc.identifier.issn1550-8080
dc.identifier.issue2en_US
dc.identifier.pmid35414498
dc.identifier.scopus2-s2.0-85128153589
dc.identifier.scopusqualityQ3
dc.identifier.startpage196en_US
dc.identifier.urihttps://hdl.handle.net/11468/20691
dc.identifier.volume52en_US
dc.identifier.wosWOS:000853675000005
dc.identifier.wosqualityQ4
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakScopus
dc.indekslendigikaynakPubMed
dc.language.isoenen_US
dc.publisherAssoc Clinical Scientistsen_US
dc.relation.ispartofAnnals of Clinical and Laboratory Science
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.subjectHn1en_US
dc.subjectCyclin B1en_US
dc.subjectDocetaxelen_US
dc.subject2-Methoxyestradiolen_US
dc.subjectApoptosisen_US
dc.titleDecreased Expression of HN1 Sensitizes Prostate Cancer Cells to Apoptosis Induced by Docetaxel and 2-Methoxyestradiolen_US
dc.titleDecreased Expression of HN1 Sensitizes Prostate Cancer Cells to Apoptosis Induced by Docetaxel and 2-Methoxyestradiol
dc.typeArticleen_US

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