甘草素对B16F10黑色素瘤细胞侵袭转移的抑制作用及其机制探讨  

INHIBITION OF LIQUIRIGENIN ON INVASION AND METASTASIS OF B16F10 MELANOMA CELLS AND THE RELATED MECHANISM

作　　者：石惠[1] 吴雨晨[1] 严淑[1] 蔡云清[1] 

机构地区：[1]南京医科大学公共卫生学院营养与食品卫生系,南京211166

出　　处：《营养学报》2014年第5期486-490,共5页Acta Nutrimenta Sinica

基　　金：国家自然科学基金(No.30972478)

摘　　要：目的研究甘草素(liquirigenin,LQ)对黑色素瘤B16F10侵袭转移的抑制作用及分子机制。方法采用四甲基氮唑兰MTT比色法检测甘草素对B16F10细胞存活力的影响;划痕实验检测甘草素对细胞迁移的影响;Transwell小室实验检测细胞侵袭能力;蛋白质印迹法分析甘草素对侵袭转移相关蛋白和信号通路的影响。结果在无毒剂量下,甘草素能明显抑制B16F10细胞的侵袭转移能力,并且随着浓度增加,其细胞的迁移和侵袭逐渐减弱;甘草素能通过抑制PI3K/AKT信号通路,下调基质金属蛋白酶MMP-2和MMP-9蛋白表达。结论甘草素可能通过阻碍PI3K/PTEN/AKT信号通路传导,下调MMP-2和MMP-9的表达,从而抑制黑色素瘤B16F10细胞的侵袭转移。Objective To study the inhibitory effect of liquiritigenin （LQ） on B16F10 melanoma invasion and metastasis, and to explore the related molecular mechanism. Methods MTT assay was used to detect the B16F10 cell viability, The effect of LQ on cell migration was measured by the scratch assay. Transwell chamber experiments were performed to detect cell invasion ability. Western blot was used to analyze the effect of LQ on metastasis-associated proteins and signaling pathway. Results In nontoxic doses, LQ could inhibit the ability of invasion and meta- stasis of B16F10 cells, with increasing concentration and the effect was gradually stronger. LQ could inhibited PI3K/ PTEN/AKT signaling pathway and decreased the matrix metalloproteinases MMP-2 and MMP-9 protein expression. Conc.lusion LQ can inhibit the invasion and metastasis of melanoma B16F10 cells possibly through the regulation of PI3K/ PTEN/AKT signaling pathway and inhibition of the expression of MMP-2 and MMP-9.

关 键 词：甘草素 黑色素瘤 侵袭 转移 

分 类 号：R739.5[医药卫生—肿瘤]