Guarnieri Tiziana
Dept. of Biology, Geology and Environmental Sciences, School of Sciences, Alma Mater Studiorum Università di Bologna, Italy, zip code: 40126, via Francesco Selmi, 3, Bologna, Italy.
Curr Cancer Drug Targets. 2016;16(2):186-97. doi: 10.2174/1568009615666150827093012.
Epidemiological data suggest that Non Steroidal Anti Inflammatory Drugs (NSAIDs) and Cyclooxygenase 2 (COX2) inhibitors (COXibs) can exert chemopreventive and antitumour effects in many human neoplasia. This is particularly true in colon cancer (CC), where the regular assumption of these molecules has been shown to exert chemopreventive and chemotherapeutic effects. Since the late '90s, there has been a progressive increase in experimental evidence, indicating that in CC the antiproliferative effects of NSAIDs and COXibs could be both dependent on and independent of COXs inhibition, and that these effects do not necessarily exclude each other. This review will examine some of these COX-independent cellular pathways, with a focus on those involved in the inhibition of CC cells proliferation through transcription factors crosstalk.
流行病学数据表明,非甾体抗炎药(NSAIDs)和环氧化酶2(COX2)抑制剂(COXibs)在许多人类肿瘤中可发挥化学预防和抗肿瘤作用。在结肠癌(CC)中尤其如此,在结肠癌中,定期服用这些分子已显示出具有化学预防和化疗作用。自20世纪90年代末以来,越来越多的实验证据表明,在结肠癌中,NSAIDs和COXibs的抗增殖作用可能既依赖于也独立于COXs抑制作用,而且这些作用不一定相互排斥。本综述将探讨其中一些不依赖COX的细胞途径,重点关注那些通过转录因子相互作用参与抑制结肠癌细胞增殖的途径。