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Fordin: A novel type I ribosome inactivating protein from Vernicia fordii modulates multiple signaling cascades leading to anti-invasive and pro-apoptotic effects in cancer cells in vitro

文献类型： 外文期刊

作者： Lu, Weili 2 ; Mao, Yingji 1 ; Chen, Xue 1 ; Ni, Jun 1 ; Zhang, Rui 1 ; Wang, Yuting 1 ; Wang, Jun 1 ; Wu, Lifang 1 ;

作者机构： 1.Chinese Acad Sci, Hefei Inst Phys Sci, Key Lab High Magnet Field & Ion Beam Phys Biol, 350 Shushanhu Rd, Hefei 230031, Anhui, Peoples R China

2.Univ Sci & Technol China, Grad Sch, Inst Tech Biol & Agr Engn, Sci Isl Branch, Hefei 230026, Anhui, Peoples R China

3.Anhui Med Univ, Sch Pharm, Anhui Key Lab Bioact Nat Prod, Hefei 230032, Anhui, Peoples R China

4.Bengbu Med Coll, Dept Life Sci, Bengbu 233030, Anhui, Peoples R China

5.Anhui Acad Agr Sci, Sericultural Res Inst, Hefei 230061, Anhui, Peoples R China

关键词： Vernicia fordii; fordin; ribosome inactivating protein; nuclear factor-B; apoptosis; invasion

期刊名称：INTERNATIONAL JOURNAL OF ONCOLOGY （ 影响因子：5.65； 五年影响因子：4.79 ）

ISSN： 1019-6439

年卷期： 2018 年 53 卷 3 期

页码：

收录情况： SCI

摘要： Fordin, which is derived from Vernicia fordii, is a novel type I ribosome inactivating protein (RIP) with RNA N-glycosidase activity. In the present study, fordin was expressed by Escherichia coli and purified using nickel affinity chromatography. Previous studies have demonstrated RIP toxicity in a variety of cancer cell lines. To understand the therapeutic potential of fordin on tumors, the present study investigated the effects of fordin on the viability of several tumor and normal cell lines. The results demonstrated that fordin induced significant cytotoxicity in four cancer cell lines, compared with the normal cell line. Specifically, profound apoptosis and inhibition of cell invasion were observed following fordin exposure in U-2 OS and HepG2 cells; however, the molecular mechanism underlying the action of RIP remains to be fully elucidated. In the present study, it was found that the anticancer effects of fordin were associated with suppression of the nuclear factor (NF)-B signaling pathway. In U-2 OS and HepG2 cells, fordin inhibited the expression of inhibitor of NF-B (IB) kinase, leading to downregulation of the phosphorylation level of IB, which quelled the nuclear translocation of NF-B. Fordin also reduced the mRNA and protein levels of NF-B downstream targets associated with cell apoptosis and metastasis, particularly B-cell lymphoma-2-related protein A1 (Blf-1) and matrix metalloproteinase (MMP)-9. The inactivation of NF-B and the reduction in the expression levels of Blf-1 and MMP-9 mediated by fordin were also confirmed by co-treatment with lipopolysaccharide or p65 small interfering RNA. These findings suggested a possible mechanism for the fordin-induced effect on tumor cell death and metastasis. The results of the present study demonstrated the multiple anticancer effects of fordin in U-2 OS and HepG2 cells, in part by inhibiting activation of the NF-B signaling pathway.

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