Please use this identifier to cite or link to this item: https://hdl.handle.net/11499/59306
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dc.contributor.authorCil, Nazli-
dc.contributor.authorOnder, Elif-
dc.contributor.authorDamar, Ayse Nur-
dc.contributor.authorTabatabaei, Seyedmahdi-
dc.contributor.authorCabus, Uemit-
dc.contributor.authorMete, Gulcin Abban-
dc.date.accessioned2025-03-22T21:38:08Z-
dc.date.available2025-03-22T21:38:08Z-
dc.date.issued2025-
dc.identifier.issn1357-0560-
dc.identifier.issn1559-131X-
dc.identifier.urihttps://doi.org/10.1007/s12032-025-02625-4-
dc.description.abstractEndometrial carcinoma, the most common malignancy of the female genital tract, remains challenging to treat despite early-stage dominance. Surgical interventions and irradiation are insufficient for advanced endometrial cancer. Our aim was to investigate to explore the in vitro cytotoxicity and apoptotic effects of boric acid (BA) on endometrial adenocarcinoma cell lines (Ishikawa and HEC-1B cell lines), providing experimental evidence for the potential application of boric acid as an anticancer drug. Time- and dose-dependent cell viability was determined with the XTT cell proliferation test. Differences in mRNA levels were determined by RT-PCR using cDNAs and SYBR green assay. Colony formation and the effect of BA on wound healing were evaluated. Immunocytochemistry and TUNEL tests were performed to evaluate apoptosis. BA increased the expression of Caspase 3 and Bax in HEC-1B and Ischikawa cell lines. It was determined that BA significantly decreased the number of colonies in both cell lines (p < 0.05). In HEC-1B and Ishikawa cell lines, there was an increase in cell migration in the control group at 16 and 24 h. The apoptotic index was higher in the BA group, although it was not statistically significant. According to immunohistochemistry results, Caspase 3 and Bax expression in HEC-1B and Ishikawa cell lines were statistically increased in BA group. The expression of Bcl-2 was decreased statistically with BA treatment in both cell lines (p = 0.0001). BA treatment inhibited cell migration and colony formation, which are important for carcinogenesis, in endometrial adenocarcinoma cell lines. This inhibition was shown to occur through the apoptotic pathway.en_US
dc.description.sponsorshipScientific and Technological Research Council of Turkiye (TUBIdot;TAK); Pamukkale University Scientific Research Projects Coordination Unit [2023HZDP002]en_US
dc.description.sponsorshipOpen access funding provided by the Scientific and Technological Research Council of Turkiye (TUB & Idot;TAK). This study was supported by The Pamukkale University Scientific Research Projects Coordination Unit (Grant 2023HZDP002).en_US
dc.language.isoenen_US
dc.publisherHumana Press incen_US
dc.rightsinfo:eu-repo/semantics/openAccessen_US
dc.subjectBoric Aciden_US
dc.subjectHec-1Ben_US
dc.subjectIshikawaen_US
dc.subjectEndometrial Adenocarcinomaen_US
dc.subjectApoptosisen_US
dc.titleIn Vitro Cytotoxic and Apoptotic Effects of Boric Acid on Endometrial Adenocarcinoma Cell Lines (Hec-1b and Ischikawa)en_US
dc.typeArticleen_US
dc.identifier.volume42en_US
dc.identifier.issue3en_US
dc.departmentPamukkale Universityen_US
dc.identifier.doi10.1007/s12032-025-02625-4-
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.authorwosidÖnder, Elif/Iqu-7845-2023-
dc.identifier.pmid39971813-
dc.identifier.scopus2-s2.0-85219163057-
dc.identifier.wosWOS:001426608700001-
dc.identifier.scopusqualityQ3-
dc.description.woscitationindexScience Citation Index Expanded-
dc.identifier.wosqualityQ3-
item.openairetypeArticle-
item.fulltextWith Fulltext-
item.cerifentitytypePublications-
item.grantfulltextopen-
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.languageiso639-1en-
crisitem.author.dept14.03. Basic Medical Sciences-
crisitem.author.dept14.03. Basic Medical Sciences-
Appears in Collections:PubMed İndeksli Yayınlar Koleksiyonu / PubMed Indexed Publications Collection
Scopus İndeksli Yayınlar Koleksiyonu / Scopus Indexed Publications Collection
Tıp Fakültesi Koleksiyonu
WoS İndeksli Yayınlar Koleksiyonu / WoS Indexed Publications Collection
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