Pro-Enflamatuvar Sitokin IL-1β'nın İnsan Akciğer Kanseri Hücrelerinde Urotensin II Gen Ekspresyonu Üzerine Etkisi

Amaç: Akciğer kanseri dünya çapında en ölümcül kanser türüdür. Akciğer kanseri hastalarının kötü prognozu ve etkili tedavinin olmaması akciğer kanseri patogenezinin ayrıntılı olarak anlaşılmasını gerektirir. Bazı çalışmalarda, U-II'nin akciğer kanseri gibi bazı hastalıkların önlenmesi ve tedavisinde olası biyobelirteç veya moleküler hedef olma durumu vurgulanmaktadır. Ancak, U-II‟nin moleküler aksiyon mekanizması henüz aydınlatılmamıştır. Bu çalışmada, akciğer kanserinde U-II'nin rolünü araştırmayı amaçladık.Gereç ve Yöntem: Çalışmamızda A549 hücre dizileri farklı doz ve sürelerde IL-1β ile uyarıldı (1, 3 ng/ml; 6, 24 saat). GAPDH, NF-κB1, MMP-1 ve U-II mRNA seviyeleri RT-qPCR yöntemi ile analiz edildi. Verilerin analizinde delta delta CT (ΔΔCt) metodu kullanıldı. Analiz edilen veriler „katlı değişim‟ olarak ifade edildi.Bulgular: Bulgularımız, A549 hücrelerinde U-II geninin eksprese edildiğini ve A549 hücrelerinde IL-1β'nın U-II, MMP-1 ve NF-κB1 gen ekspresyonlarını indükleyebildiğini göstermektedir.Sonuç: U-II, akciğer kanseri tedavisinde ve önlenmesinde umut verici bir moleküler hedeftir. Bu nedenle, akciğer adenokarsinomasında U-II'nin moleküler mekanizmasını aydınlatmak için daha ileri çalışmalara ihtiyaç vardır.

Effect of Pro-Inflammatory Cytokine IL-1β, on Urotensin II Gene Expression in Human Lung Cancer Cells

Objective: Lung cancer is the deadliest cancer type world-wide. Poor prognosis of lung cancer patients and lack of an effective treatment require detailed understanding of lung cancer pathogenesis. It was highlighted in some studies that U-II is likely to be a biomarker or molecular target for the prevention and treatment of some diseases such as lung cancer. But its molecular action mechanism has not been elucidated yet. In the present study, we aimed to investigate the role of U-II in lung cancer.Methods: In our study, A549 cells were induced with different doses of IL-1β at different durations (1, 3 ng/ml; 6, 24 hours). mRNA levels of GAPDH, NF-κB1, MMP-1, and U-II were analyzed with RT-qPCR. The Delta Delta Ct (ΔΔCt) method was used for data analysis. The analyzed data were expressed as the “fold-change”.Results: Our results indicate that U-II gene is expressed in A549 cells and IL-1β can induce gene expressions of U-II, MMP-1 and NF-κB1 in A549 cells.Conclusions: U-II is a promising molecular target in treatment and prevention of lung cancer. Therefore, further studies are needed to enlighten molecular mechanism of U-II in lung adenocarcinoma.

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KONURALP TIP DERGİSİ-Cover
  • ISSN: 1309-3878
  • Yayın Aralığı: Yılda 3 Sayı
  • Başlangıç: 2009
  • Yayıncı: Düzce Üniversitesi Tıp Fakültesi Aile Hekimliği AD adına Yrd.Doç.Dr.Cemil Işık Sönmez
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