Apoptotic Effects of Etodolac in Breast Cancer Cell Cultures


Creative Commons License

Orun O. , Mega Tiber P., Koçyiğit Sevinç S.

Nonsteroidal Anti-Inflammatory Drugs, Ali Gamal Ahmed Al-kaf, Editör, IntechOpen, Rijeka, ss.133-151, 2017

  • Yayın Türü: Kitapta Bölüm / Araştırma Kitabı
  • Basım Tarihi: 2017
  • Yayınevi: IntechOpen
  • Basıldığı Şehir: Rijeka
  • Sayfa Sayıları: ss.133-151
  • Editörler: Ali Gamal Ahmed Al-kaf, Editör

Özet

Nonsteroidal anti‐inflammatory drugs (NSAIDs) are commonly used as anti‐inflammatory

and analgesic agents. This family of drugs suppresses prostaglandin synthesis through

inhibition of cyclooxygenase (COX) enzymes. Recent studies displayed that anti‐carcinogenic

actions of these drugs are mediated by COX‐2 enzyme. Currently, there is intense

research on COX‐2 inhibitors as therapeutic targets. Etodolac is not perfectly selective

but shows ‘preferential selectivity’ for COX‐2. Here, in this study, we wanted to take

gene expression snapshots of several apoptotic proteins under different conditions of

drug exposure. The aim, therefore, focused to determine differential effects of etodolac

on the regulation of apoptotic genes in hormone‐responsive MCF‐7 and triple‐negative

MDA‐MB‐231 cancer cell lines. Our data suggest that MDA‐MB‐231 is more responsive

to etodolac exposure. Cell proliferation and apoptosis consistently regulated upon drug

addiction. Furthermore, COX‐2/HER2 was explicitly an up‐regulated, phosphorylated

form of Bad accumulated and anti‐apoptotic proteins SAG and survivin increased in both

transcriptional and translational levels. Changes in mitochondrial Bcl‐2 family proteins

were moderate and pro‐ and anti‐apoptotic proteins showed similar levels of regulation

in both cell lines. We believe that these findings would be supportive for future studies

targeting etodolac‐based therapies, as it reveals apoptotic factors differentially regulated

in hormone‐responsive and invasive cell lines