肝细胞癌(HCC)患者的总生存时间很短,目前尚无有效的全身治疗药物。环氧化酶-2(COX-2)在大多数恶性肿瘤(包括HCC)中都存在过表达。研究显示,COX-2抑制剂通过抑制前列腺素E2(PGE2)合酶的活性,发挥抗HCC作用,但效果有限,长期用药不良反应大。PGE2与不同的前列腺素受体(EPR)作用产生效应,对肝脏的生理和病理功能起到重要调节作用,而EPR在介导PGE2信号的传递中起到重要作用,可能为HCC的治疗提供新的思路。文中综述PGE及其受体对肝脏功能的调节作用及PGE2-EPR信号转导在HCC发生中的作用与机制,将为开发有效的抗肿瘤药物提供新的治疗策略。
To date, no effective systemic chemotherapeutic or chemopreventive treatments are available; thus, innovative treatment approaches are urgently needed. There is compelling evidence that eyelooxygenase-2 (COX-2) is overexpressed in a multitude of malignancies including hepatoeellular carcinoma (HCC) , and selective COX-2 inhihitors reducing prostaglandin E2 (PGE2) signaling exert antitumorigenie effect in HCC cells. However, selective COX-2 inhibitors are not free of unwanted side effects. Acting via differentially regulated E-prostanold receptors (EPR) , PGE2 plays an important role in the liver. This review summarized the recent advances in understanding the function and the mechanism for PGE2-EPR signaling pathway in hepatocareinogenesis, which will contribute to develop more effective chemopreventive and therapeutic strategies.