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癌-睾丸抗原MAGE-C2结合Rbx1并抑制泛素连接酶介导的细胞周期蛋白E的周转。

Cancer-testis antigen MAGE-C2 binds Rbx1 and inhibits ubiquitin ligase-mediated turnover of cyclin E.

作者信息

Hao Jiaqing, Song Xiao, Wang Jingjing, Guo Chengli, Li Yan, Li Bing, Zhang Yu, Yin Yanhui

机构信息

Department of Immunology, School of Basic Medical Sciences, Peking University Health Science Center, Beijing, China.

Department of Microbiology and Immunology, University of Louisville, Louisville, Kentucky, USA.

出版信息

Oncotarget. 2015 Dec 8;6(39):42028-39. doi: 10.18632/oncotarget.5973.

DOI:10.18632/oncotarget.5973
PMID:26540345
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4747207/
Abstract

Cancer-testis antigen MAGE-C2 is normally expressed in testis but aberrantly expressed in various kinds of tumors. Its functions in tumor cells are mostly unknown. Here, we show that MAGE-C2 binds directly to the RING domain protein Rbx1, and participates in Skp1-Cullin1-F box protein (SCF) complex. Furthermore, MAGE-C2 can inhibit the E3 ubiquitin ligase activity of SCF complex. Ablation of endogenous MAGE-C2 decreases the level of cyclin E and accelerates cyclin E turnover by inhibiting ubiquitin-mediated proteasome degradation. Overexpression of MAGE-C2 increases the level of cyclin E and promotes G1-S transition and cell proliferation, and the results are further confirmed by knockdown of MAGE-C2. Overall, the study indicates that MAGE-C2 is involved in SCF complex and increases the stability of cyclin E in tumor cells.

摘要

癌-睾丸抗原MAGE-C2通常在睾丸中表达，但在各种肿瘤中异常表达。其在肿瘤细胞中的功能大多未知。在此，我们表明MAGE-C2直接与RING结构域蛋白Rbx1结合，并参与Skp1-Cullin1-F盒蛋白（SCF）复合物。此外，MAGE-C2可抑制SCF复合物的E3泛素连接酶活性。内源性MAGE-C2的缺失会降低细胞周期蛋白E的水平，并通过抑制泛素介导的蛋白酶体降解加速细胞周期蛋白E的周转。MAGE-C2的过表达会增加细胞周期蛋白E的水平，并促进G1-S期转换和细胞增殖，MAGE-C2的敲低进一步证实了这些结果。总体而言，该研究表明MAGE-C2参与SCF复合物，并增加肿瘤细胞中细胞周期蛋白E的稳定性。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/55c7/4747207/20af445072af/oncotarget-06-42028-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/55c7/4747207/5315d3898976/oncotarget-06-42028-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/55c7/4747207/f2c96625c9df/oncotarget-06-42028-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/55c7/4747207/90487ef8618b/oncotarget-06-42028-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/55c7/4747207/f04766272294/oncotarget-06-42028-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/55c7/4747207/d14940d31163/oncotarget-06-42028-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/55c7/4747207/f52d9b9a55ac/oncotarget-06-42028-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/55c7/4747207/20af445072af/oncotarget-06-42028-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/55c7/4747207/5315d3898976/oncotarget-06-42028-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/55c7/4747207/f2c96625c9df/oncotarget-06-42028-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/55c7/4747207/90487ef8618b/oncotarget-06-42028-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/55c7/4747207/f04766272294/oncotarget-06-42028-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/55c7/4747207/d14940d31163/oncotarget-06-42028-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/55c7/4747207/f52d9b9a55ac/oncotarget-06-42028-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/55c7/4747207/20af445072af/oncotarget-06-42028-g007.jpg

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