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