The rational design and synthesis of eight newly developed pyrazole-based compounds derived from ar-turmerone aimed at enhancing COX-2 inhibition and antiproliferative activity against CRC highlight the potential of pyrazole-based ar-turmerone analogs as promising lead candidates for selective COX-2 inhibition and targeted therapy in inflammation-associated colorectal cancer.
Abstract
Colorectal cancer (CRC) is still one of the most common cancers responsible for a high number of deaths globally, with chronic inflammation recognized as a pivotal factor in its pathogenesis. Cyclooxygenase-2 (COX-2) is frequently overexpressed and is a key contributor to tumor development and progression through inflammatory pathways. Ar-turmerone, a natural derived from Curcuma longa, possesses modest anti-inflammatory and antiproliferative properties; however, its therapeutic efficacy is limited compared to established COX-2 inhibitors, celecoxib. In this study, the rational design and synthesis of eight newly developed pyrazole-based compounds derived from ar-turmerone aimed at enhancing COX-2 inhibition and antiproliferative activity against CRC. Molecular docking revealed favorable COX-2 binding, especially for compounds 3e and 3f. Enzyme-based assays confirmed their potent and selective COX-2 inhibition (IC50 = 0.63 µM, SI = 14.38 and 1.04 µM, SI = 23.57, respectively). Furthermore, an antiproliferative assay in HT-29 cells revealed significant effects, with GI50 values of 5.85 µM (3e) and 9.57 µM (3f). Western blot analysis showed marked downregulation of COX-2 and suppression on phosphor-ERK and then leading to downregulation of key proliferation markers, including PCNA and Cyclin D1. Notably, co-treatment with exogenous PGE2 attenuated the antiproliferative effects, implicating the COX-2–PGE2–ERK1/2 signaling axis in CRC cell survival under inflammatory conditions. These findings highlight the potential of pyrazole-based ar-turmerone analogs, particularly compounds 3e and 3f, as promising lead candidates for selective COX-2 inhibition and targeted therapy in inflammation-associated colorectal cancer.
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