ktd Kocatepe Tıp Dergisi 3061-9904 Afyonkarahisar Sağlık Bilimleri Üniversitesi 10.18229/kocatepetip.1683292 Urology Üroloji BORAKS PROSTAT KANSERİ HÜCRELERİNDE OTOFAJİ YOLAĞINI REGÜLE EDEREK PROLİFERASYONU ENGELLER Borax Inhibits Proliferation by Regulating the Autophagy Pathway in Prostate Cancer Cells https://orcid.org/0000-0001-8319-512X Başaran Ekrem DÜZCE ÜNİVERSİTESİ https://orcid.org/0000-0002-0993-6118 Hacıoğlu Ceyhan Düzce Üniversitesi https://orcid.org/0000-0003-2869-9629 Uyurca Sare DÜZCE ÜNİVERSİTESİ https://orcid.org/0000-0002-4779-6777 Baba Dursun DÜZCE ÜNİVERSİTESİ https://orcid.org/0000-0003-4556-3475 Taşkıran Arda Taşkın DÜZCE ÜNİVERSİTESİ https://orcid.org/0000-0001-8051-5802 Balık Ahmet Yıldırım DÜZCE ÜNİVERSİTESİ 04 16 2026 27 2 175 181 04 24 2025 08 21 2025 Copyright © 1999, Kocatepe Tıp Dergisi 1999 Kocatepe Tıp Dergisi

AMAÇ: Otofaji, kanser hücrelerinin hayatta kalmasında ve te-daviye karşı direnç geliştirmesinde kritik bir rol oynamaktadır. Esansiyel bir iz element olan bor, çeşitli biyolojik süreçlerde yer almaktadır; ancak, prostat kanserinde boraksın antitümör etki-leri üzerine yapılan araştırmalar sınırlı olup, bu bağlamda otofa-jinin rolü hâlen yeterince anlaşılmamıştır. Bu çalışma, boraksın DU-145 insan prostat kanseri hücrelerinde otofaji üzerindeki etkilerini ve bu etkilerin moleküler düzeydeki mekanizmaları araştırılmıştır.GEREÇ VE YÖNTEM: : DU-145 hücreleri in vitro koşullarda kültürlenmiş ve boraks ile muamele edilmiştir. Hücre canlılığı ve proliferasyonu, MTT (3-(4,5-dimetiltiazol-2-il)-2,5-difenil-tetrazolyum bromür) testi ve BrdU (5-bromo-2'-deoksiüridin) inkorporasyon yöntemi ile değerlendirilmiştir. Sitotoksik bo-raks konsantrasyonları belirlendikten sonra, otofaji ile ilişkili belirteçler olan Beclin1, mikrotübül ilişkili protein 1 hafif zincir 3 (LC3-II) ve sequestosome-1 (SQSTM1) ekspresyon düzeyleri ölçülmüştür.BULGULAR: Elde edilen sonuçlar, boraksın DU-145 hücre canlı-lığını doz bağımlı olarak anlamlı biçimde azalttığını göstermiş-tir. Ayrıca, boraks hücre proliferasyonunu baskılamış ve hücre döngüsünün S fazındaki hücre oranını önemli ölçüde azaltmış-tır. Moleküler düzeyde ise boraks uygulaması, SQSTM1’in azal-masına, Beclin1 ve LC3-II’nin ise artmasına yol açarak otofajinin indüklendiğine işaret etmiştir.SONUÇ: Bu bulgular, boraksın DU-145 prostat kanseri hücre-lerinin proliferasyonunu otofajik yolakları aktive ederek inhibe ettiğini göstermektedir. Gözlemlenen etkilerin, büyük ölçüde Beclin1/LC3-II/SQSTM1 sinyal yolunun modülasyonu ile ilişkili olduğu düşünülmektedir. Ayrıca, boraksın bir otofaji aktivatö-rü ile kombinasyonu, antitümör etkinliğini artırabilir ve prostat kanseri tedavisinde umut verici bir strateji sunabilir.

OBJECTIVE: Autophagy plays a critical role in the survival of cancer cells and the development of resistance to therapeutic agents. Boron, an essential trace element, is involved in various biological processes; however, limited research has investigated the antitumor effects of borax in prostate cancer, and the role of autophagy in this context remains inadequately understood. The present study investigated the effects and underlying mechanisms of borax on autophagy in DU-145 human prostate cancer cells.MATERIAL AND METHODS: DU-145 cells were cultured in vitro and treated with borax. Cell viability and proliferation were assessed using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay and the 5-bromo-2'-deoxyuridine (BrdU) incorporation method. Following the determination of cytotoxic borax concentrations, the expression levels of autophagy-related markers Beclin1, microtubule-associated protein 1 light chain 3 (LC3-II), and sequestosome-1 (SQSTM1) were measured.RESULTS: The results demonstrated that borax significantly reduced DU-145 cell viability in a dose-dependent manner. Moreover, borax suppressed cell proliferation and markedly decreased the proportion of cells in the S phase of the cell cycle. At the molecular level, borax treatment led to a reduction of SQSTM1 and an increase of Beclin1 and LC3-II, indicating the induction of autophagy.CONCLUSIONS: These findings suggest that borax inhibits the proliferation of DU-145 prostate cancer cells by activating autophagic pathways. The observed effects appear to be mediated through the modulation of the Beclin1/LC3-II/SQSTM1 signaling axis. Furthermore, the combination of borax with an autophagy activator may enhance its antitumor efficacy, presenting a promising strategy for therapeutic intervention in prostate cancer.

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