American Association for Cancer Research
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Supplementary Figure S4 from The Ubiquitin-like Protein FAT10 Stabilizes eEF1A1 Expression to Promote Tumor Proliferation in a Complex Manner

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posted on 2023-03-31, 00:13 authored by Xiuxia Liu, Leifeng Chen, Jin Ge, Chen Yan, Zixi Huang, Junwen Hu, Chongyu Wen, Ming Li, Da Huang, Yumin Qiu, Haibin Hao, Rongfa Yuan, Jun Lei, Xin Yu, Jianghua Shao

Supplementary Fig. S4 FAT10 stabilizes eEF1A1 protein levels by attenuating eEF1A1 ubiquitination and degradation in cancer cells.

Funding

National Natural Science Foundation of China

Jiangxi Provincial Department of Science and Technology

Project of Jiangxi Provincial Department of Education

History

ARTICLE ABSTRACT

Human HLA-F adjacent transcript 10 (FAT10) is the only ubiquitin-like protein that can directly target substrates for degradation by proteasomes, but it can also stabilize the expression of certain substrates by antagonizing ubiquitination, through mechanisms as yet uncharacterized. In this study, we show how FAT10 stabilizes the translation elongation factor eEF1A1, which contributes to cancer cell proliferation. FAT10 overexpression increased expression of eEF1A1, which was sufficient to promote proliferation of cancer cells. Mechanistic investigations revealed that FAT10 competed with ubiquitin (Ub) for binding to the same lysines on eEF1A1 to form either FAT10–eEF1A1 or Ub–eEF1A1 complexes, respectively, such that FAT10 overexpression decreased Ub–eEF1A1 levels and increased FAT10–eEF1A1 levels. Overall, our work establishes a novel mechanism through which FAT10 stabilizes its substrates, advancing understanding of the biological function of FAT10 and its role in cancer. Cancer Res; 76(16); 4897–907. ©2016 AACR.