Prostate Cancer Progression: Aspirin Induces Toxicity in Prostate Cancer Cell

Olaniyi Ogundiya, Helen Whiteland, U. K. Shah, O. Bodger, J. Verma, H. Haboubi, B. Rees, H. Kynaston, S. Doak

Research output: Contribution to journalArticlepeer-review

21 Citations (Scopus)

Abstract

Introduction: Aspirin has shown a great promise in the management of cancer. Evidence from colorectal cancer studies suggests that the antitumor properties of aspirin are due to the direct inhibition of cyclooxygenase-2 (COX-2) activity. Such evidence are lacking in prostate cancer. In our previous study, we reported that prostate cancer cell express high levels of COX-2. Therefore, we evaluated the role of aspirin in prostate cancer progression. Aim: To assess the toxicity of aspirin and it active metabolite, sodium salicylate in prostate cell. Method: We exposed PNT2 (normal prostate), DU145 (prostatic brain metastasis), PC3 (prostatic bone metastasis) to six physiologically relevant doses (0- 10mM) of aspirin and sodium salicylate. Relative population doubling (RPD) was applied to provide a quantitative measure of cell growth, death and cytostasis. Result: We observed that sodium salicylate was most potent in PC-3 cells, the most aggressive cell line and least potent in PNT2 (normal prostate cell). LC50 values were 8.5mM, 9.2mM and 13.2mM for PC3, DU145 and PNT2 respectively. With aspirin, prostatic cancer cell lines (PC-3, DU-145) showed highly significant toxicity response compared to normal prostate cell (PNT2) from 6mM (p<0.0001). Conclusion: This study provides evidence that aspirin has a role in prostate cancer progression
Original languageEnglish
Pages (from-to)S13
JournalInternational Journal of Surgery
Volume47
Issue numberS1
DOIs
Publication statusPublished - 30 Nov 2017

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