Abstract

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 showed that anti-carcinogenic effects of these drugs are especially mediated by COX-2 enzyme. Etodolac is a COX-2 inhibitor and though not perfectly selective, it exhibits “preferential selectivity” for COX-2. In this study, the anti-proliferative and apoptotic effects of etodolac and its hydrazone or triazole derivatives (SGK 206 and SGK 242, respectively), were investigated on prostate cancer cell line PC-3 and human colorectal carcinoma cell line HT-29. Our data showed that SGK 206 and SGK 242 were more effective in the inhibition of proliferation and induction of apoptosis compared to etodolac in both cell lines.

Highlights

  • Nonsteroidal anti-inflammatory drugs (NSAIDs), regularly used for their anti-inflammatory and analgesic effects, were shown to have potency for cancer prevention as well [1]

  • Reports about the role of NSAIDs in cancer were from the studies on colorectal cancer (CRC)

  • We focused on the anti-carcinogenic effects of etodolac and its hydrazone and triazole derivatives (SGK 206 and SGK 242, respectively) in two cancer cell lines

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Summary

Introduction

Nonsteroidal anti-inflammatory drugs (NSAIDs), regularly used for their anti-inflammatory and analgesic effects, were shown to have potency for cancer prevention as well [1]. Its toxicity and relative selectivity for COX-2 is low, and there are numerous studies about its anti-carcinogenic activity, dose-response relationship on various cancer cell lines are not well established. We focused on the anti-carcinogenic effects of etodolac and its hydrazone and triazole derivatives (SGK 206 and SGK 242, respectively) in two cancer cell lines. Cell viability and growth inhibition were determined using MTT colorimetric assay, according to the instructions of manufacturer

Results
Conclusion

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