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在黑色素瘤模型中,SKLB-M8通过AKT/mTOR信号通路诱导细胞凋亡,并通过降低ERK1/2磷酸化来抑制血管生成。

SKLB-M8 induces apoptosis through the AKT/mTOR signaling pathway in melanoma models and inhibits angiogenesis with decrease of ERK1/2 phosphorylation.

作者信息

Wang Jingjing, Yang Zhuang, Wen Jiaolin, Ma Feng, Wang Fang, Yu Kun, Tang Minghai, Wu Wenshuang, Dong Yinfeng, Cheng Xia, Nie Chunlai, Chen Lijuan

机构信息

State Key Laboratory of Biotherapy, West China Hospital, West China Medical School, Sichuan University, China.

出版信息

J Pharmacol Sci. 2014;126(3):198-207. doi: 10.1254/jphs.14077fp. Epub 2014 Oct 21.

Abstract

SKLB-M8, a derivative of millepachine, showed significant anti-proliferative effects in melanoma cell lines. In this study, we investigated the anti-melanoma and anti-angiogenic activity of SKLB-M8 on three melanoma cell lines (A2058, CHL-1, and B16F10) and human umbilical vein endothelial cells (HUVECs). In vitro, SKLB-M8 showed anti-proliferative activity with IC50 values of 0.07, 0.25, and 0.88 μM in A2058, CHL-1, and B16F10 cell lines, respectively. Flow cytometory analysis showed that SKLB-M8 induced G2/M arrest in three melanoma cell lines, and western blotting demonstrated that SKLB-M8 down-regulated the expression of cdc2, up-regulated p53 in A2058 and CHL-1 cells, and triggered cell apoptosis through down-regulating AKT and phosphorylated mTOR (p-mTOR). SKLB-M8 also inhibited HUVEC proliferation, migration, invasion, and tube formation in vitro with the inhibition of phosphorylated ERK1/2 (p-ERK1/2). In vivo, alginate-encapsulated tumor cell assay revealed that SKLB-M8 suppressed B16F10 tumor angiogenesis. In CHL-1- and B16F10-tumor-bearing mouse models, SKLB-M8 inhibited tumor growth by oral treatment with less toxicity. CD31 immunofluoresence staining and caspase-3 immunohistochemistry indicated that SKLB-M8 inhibited melanoma tumor growth by targeting angiogenesis and inducing caspase3-dependent apoptosis. SKLB-M8 might be a potential anti-melanoma drug candidate.

摘要

SKLB-M8是一种楝叶吴茱萸碱衍生物,对黑色素瘤细胞系显示出显著的抗增殖作用。在本研究中,我们研究了SKLB-M8对三种黑色素瘤细胞系(A2058、CHL-1和B16F10)以及人脐静脉内皮细胞(HUVEC)的抗黑色素瘤和抗血管生成活性。在体外,SKLB-M8在A2058、CHL-1和B16F10细胞系中分别显示出抗增殖活性,IC50值分别为0.07、0.25和0.88 μM。流式细胞术分析表明,SKLB-M8在三种黑色素瘤细胞系中诱导G2/M期阻滞,蛋白质免疫印迹法表明,SKLB-M8下调A2058和CHL-1细胞中cdc2的表达,上调p53的表达,并通过下调AKT和磷酸化mTOR(p-mTOR)触发细胞凋亡。SKLB-M8还通过抑制磷酸化ERK1/2(p-ERK1/2)在体外抑制HUVEC的增殖、迁移、侵袭和管腔形成。在体内,海藻酸钠包封的肿瘤细胞试验表明,SKLB-M8抑制B16F10肿瘤血管生成。在携带CHL-1和B16F10肿瘤的小鼠模型中,SKLB-M8通过口服给药抑制肿瘤生长,且毒性较小。CD31免疫荧光染色和caspase-3免疫组化表明,SKLB-M8通过靶向血管生成和诱导caspase3依赖性凋亡来抑制黑色素瘤肿瘤生长。SKLB-M8可能是一种潜在的抗黑色素瘤候选药物。

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