A comparison of the effectiveness of selected non-steroidal anti-inflammatory drugs and their derivatives against cancer cells in vitro

Abstract

The method of chemotherapy (i.e., intravascular, intrathecal, oral) might dictate the choice of NSAID/NSAID derivative used to treat/prevent a given type of cancer. Also, the p75 NTR tumor suppressor appears to be a common molecular mechanism that mediates the growth inhibiting effectiveness of these drugs.

Supramolecular Chiro-Biomedical Assays and Enantioselective HPLC Analyses for Evaluation of Profens as Non-Steroidal Anti-Inflammatory Drugs, Potential Anticancer Agents and Common Xenobiotics

“…In nested case-control study Daugherty et al [34] observed that risks of prostate cancer were significantly reduced among regular ibuprofen users who carried allele variants at four non-synonymous single nucleotide polymorphism (nsSNP) loci of the -methylacyl-CoA-racemase (AMACR) gene and carried TGTGCG haplotype. Overexpression of AMACR, which is implicated in the activation of the COX-inhibiting form of ibuprofen, has been commonly observed in prostate cancer subjects [34,38]. Similarly, overexpression of COX-2 and increased prostaglandin biosynthesis correlates with carcinogenesis and metastasis at most anatomic sites [36].…”

“…In case of prostate cancer and ovarian cancer lines the up-regulation of the p75 NTR tumor suppressor which appears to be a common molecular mechanism that mediates the growth inhibiting effectiveness of these drugs [34,36,38]. Andrews et al [38] reveals that R-flurbiprofen and R-ibuprofen were most effective at clinically relevant dosages over the nitric oxide-linked aspirin and celecoxib to inhibit the growth of different human cancer cells including cell lines expressing multidrug resistance-1 -glycoprotein (MDR-1).…”

“…In case of prostate cancer and ovarian cancer lines the up-regulation of the p75 NTR tumor suppressor which appears to be a common molecular mechanism that mediates the growth inhibiting effectiveness of these drugs [34,36,38]. Andrews et al [38] reveals that R-flurbiprofen and R-ibuprofen were most effective at clinically relevant dosages over the nitric oxide-linked aspirin and celecoxib to inhibit the growth of different human cancer cells including cell lines expressing multidrug resistance-1 -glycoprotein (MDR-1). In nested case-control study Daugherty et al [34] observed that risks of prostate cancer were significantly reduced among regular ibuprofen users who carried allele variants at four non-synonymous single nucleotide polymorphism (nsSNP) loci of the -methylacyl-CoA-racemase (AMACR) gene and carried TGTGCG haplotype.…”

“…Profens, together with nitric oxide-linked NSAIDs and their derivatives, recently have received significant attention with regard to their anti-cancer effectiveness and have been selected for advanced clinical trials to treat a variety of human cancers [34][35][36][37][38]. In case of prostate cancer and ovarian cancer lines the up-regulation of the p75 NTR tumor suppressor which appears to be a common molecular mechanism that mediates the growth inhibiting effectiveness of these drugs [34,36,38].…”

Optimization of the mobile phase composition for preparative chiral separation of flurbiprofen enantiomers

“…This interest is based on the fact that his R enantiomer has been referred as a promoter of efficient inhibition on the development of varied forms of cancer in human beings [2], such as, the prostate cancer [3][4][5] and the colon cancer [6,7]. The most recent application area of flurbiprofen enantiomers has been described in numerous clinic and pharmacological reports, in which the R enantiomer is referred as an important hypothetical drug used to minimize the progression of Alzheimer disease [8][9][10][11].…”