CAPSAICIN SUPPRESSES CELL VIABILITY BY REGULATING EPITHELIAL-MESENCHYMAL TRANSITION IN U87 HUMAN GLIOBLASTOMA CELLS

Year 2024, Volume: 33 Issue: 2, 271 - 278, 25.07.2024

Ceyhan Hacıoğlu

https://doi.org/10.34108/eujhs.1405234

Abstract

Glioblastomastands out as one of the most prevalent malignant tumors affecting the central nervous system, and its current prognosis is unfavorable due to the lack of effective treatment options. Capsaicin, a derivative of homovanillic acid, has been documented for its anti-tumor effects across various cancer cell lines. Epithelial-to-mesenchymal transition is a pivotal molecular and cellular process inherent to normal embryogenesis and wound healing. Moreover, it plays a widespread role in diverse carcinoma and glioblastoma types. This study sought to explore the potential involvement of epithelial-to-mesenchymal transition in the anti-tumor effects induced by capsaicin in U87 glioblastoma cell lines. Initially, the impact of capsaicin treatment on cell viability was assessed through 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide analysis. Subsequently, cellular proliferation and cytotoxicity were evaluated using bromodeoxyuridine analysis. Further examinations involved determining the levels of N-cadherin, matrix metalloproteinase-9, vimentin, transforming growth factor β, caspase 3, cytochrome c, glutathione reductase, malondialdehyde and catalase through enzyme-linked immunosorbent assay. Capsaicin exhibited anti-proliferative effects in U87 cells, displaying a concentration-dependent reduction in cell viability, particularly with concentrations exceeding 50 μM. Additionally, capsaicin administration led to decreased of N-cadherin, matrix metalloproteinase-9, vimentin, transforming growth factor β, glutathione reductase and catalaselevels in U87 cells, while increasing caspase 3, cytochrome c and malondialdehyde levels.Our results showed that capsaicin treatment not only regulates epithelial-to-mesenchymal transition in U87 cells, but also suppresses cell viability by triggering apoptotic and oxidative processes. This observation suggests that epithelial-to-mesenchymal transition plays a pivotal role in the proliferation and migration of glioblastoma. Consequently, targeting this capsaicin-mediated signaling pathway could be considered a promising therapeutic approach in the treatment of glioblastoma.

Keywords

Epithelial-mesenchymal transition, glioblastoma, capsaicin

KAPSAİSİN U87 İNSAN GLİOBLASTOMA HÜCRELERİNDE EPİTELYAL-MEZENKİMAL GEÇİŞİ REGÜLE EDEREK HÜCRE CANLILIĞINI BASKILAR

Abstract

Glioblastoma, merkezi sinir sistemini etkileyen en yaygın malign tümörlerden biri olarak öne çıkmakta ve etkili tedavi seçeneklerinin bulunmaması nedeniyle mevcut prognozu kötüdür. Homovanilik asidin bir türevi olan kapsaisinin, çeşitli kanser hücre dizileri üzerindeki anti-tümör etkileri belgelenmiştir. Epitelyal-mezenkimal geçiş, normal embriyogenez ve yara iyileşmesinin doğasında bulunan önemli bir moleküler ve hücresel süreçtir. Ayrıca çeşitli karsinom ve glioblastoma tiplerinde yaygın bir rol oynar. Bu çalışma, U87 glioblastoma hücre hatlarında kapsaisin tarafından indüklenen anti-tümör etkilerine epitelyal-mezenkimal geçişin potansiyel katılımını araştırmayı amaçladı. Başlangıçta kapsaisin tedavisinin hücre canlılığı üzerindeki etkisi 3-(4,5-dimetiltiyazol-2-il)-2,5-difenil tetrazolyum bromür analizi yoluyla değerlendirildi. Daha sonra hücresel proliferasyon ve sitotoksisite, bromodeoksiüridin analizi kullanılarak değerlendirildi. Daha ileri incelemeler, enzim-bağlı immünosorbent deneyi yoluyla N-kaderin, matriks metalloproteinaz-9, vimentin, transforme edici büyüme faktörü β, kaspaz 3, sitokrom c, glutatyon redüktaz, malondialdehit ve katalaz seviyelerinin belirlenmesini içeriyordu. Kapsaisin, U87 hücrelerinde anti-proliferatif etkiler sergileyerek, özellikle 50 μM'yi aşan konsantrasyonlarda hücre canlılığında konsantrasyona bağlı bir azalma sergiledi. Ek olarak kapsaisin uygulaması, U87 hücrelerinde N-kaderin, matriks metalloproteinaz-9, vimentin, transforme edici büyüme faktörü β, glutatyon redüktaz ve malondialdehit seviyelerinin azalmasına yol açarken, kaspaz 3, sitokrom c ve malondialdehit seviyelerinin artışına neden olmuştur.Sonuçlarımız kapsaisin uygulamasının U87 hücrelerinde epitelyal-mezenkimal geçişi düzenlemesinin yanı sıra apoptotik ve oksidatif süreçleri de tetikleyerek hücre canlılığını baskıladığını göstermiştir. Bu gözlem, epitelyal-mezenkimal geçişinglioblastoma çoğalmasında ve migrasyonunda önemli bir rol oynadığını göstermektedir. Sonuç olarak, kapsaisin aracılı bu sinyal yolunun hedeflenmesi, glioblastoma tedavisinde umut verici bir terapötik yaklaşım olarak düşünülebilir.

Keywords

Epitelyal-mezenkimal geçiş, glioblastoma, kapsaisin

Ethical Statement

Ticari olarak temin edilen hücre hatları in vitro çalışma olarak kullanıldığı için etik onay gerekmemektedir.

Supporting Institution

Bu çalışma herhangi bir fon tarafından desteklenmemiştir.

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