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Review
. 2022 May 6;13(5):831.
doi: 10.3390/genes13050831.

USP10 as a Potential Therapeutic Target in Human Cancers

Li Tao  1 , Xiao Liu  2 , Xinya Jiang  2 , Kun Zhang  2 , Yijing Wang  2 , Xiumin Li  3 , Shulong Jiang  4 , Tao Han  2   3
Affiliations
Review

USP10 as a Potential Therapeutic Target in Human Cancers

Li Tao et al. Genes (Basel). .

Abstract

Deubiquitination is a major form of post-translational protein modification involved in the regulation of protein homeostasis and various cellular processes. Deubiquitinating enzymes (DUBs), comprising about five subfamily members, are key players in deubiquitination. USP10 is a USP-family DUB featuring the classic USP domain, which performs deubiquitination. Emerging evidence has demonstrated that USP10 is a double-edged sword in human cancers. However, the precise molecular mechanisms underlying its different effects in tumorigenesis remain elusive. A possible reason is dependence on the cell context. In this review, we summarize the downstream substrates and upstream regulators of USP10 as well as its dual role as an oncogene and tumor suppressor in various human cancers. Furthermore, we summarize multiple pharmacological USP10 inhibitors, including small-molecule inhibitors, such as spautin-1, and traditional Chinese medicines. Taken together, the development of specific and efficient USP10 inhibitors based on USP10's oncogenic role and for different cancer types could be a promising therapeutic strategy.

Keywords: USP10; deubiquitinating enzymes (DUBs); inhibitors; therapeutic strategy; tumorigenesis.

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Conflict of interest statement

The authors declare no conflict of interests.

Figures

Figure 1
Figure 1
Schematic illustration of ZnF, UIM, and UBA subfamily architectures.
Figure 2
Figure 2
Schematic illustration of UBL-related subfamily architectures.
Figure 3
Figure 3
Schematic illustration of USP10-related subfamily architectures.
Figure 4
Figure 4
USP10 targets different signaling pathways in cancer cells.
See this image and copyright information in PMC

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References

    1. Hershko A., Ciechanover A. The ubiquitin system. Annu. Rev. Biochem. 1998;67:425–479. doi: 10.1146/annurev.biochem.67.1.425. - DOI - PubMed
    1. Kleiger G., Mayor T. Perilous journey: A tour of the ubiquitin–proteasome system. Trends Cell Biol. 2014;24:352–359. doi: 10.1016/j.tcb.2013.12.003. - DOI - PMC - PubMed
    1. Friedberg E.C. Reversible Monoubiquitination of PCNA: A Novel Slant on Regulating Translesion DNA Synthesis. Mol. Cell. 2006;22:150–152. doi: 10.1016/j.molcel.2006.04.002. - DOI - PubMed
    1. Çetin G., Klafack S., Studencka-Turski M., Krüger E., Ebstein F. The Ubiquitin–Proteasome System in Immune Cells. Biomolecules. 2021;11:60. doi: 10.3390/biom11010060. - DOI - PMC - PubMed
    1. Baek K.-H. Conjugation and deconjugation of ubiquitin regulating the destiny of proteins. Exp. Mol. Med. 2003;35:1–7. doi: 10.1038/emm.2003.1. - DOI - PubMed

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Grants and funding

T.H. was supported in part by the Henan National Science Fund for Excellent Young Scholars (No. 212300410067), the National Natural Science Foundation of China (Nos. 82002731 and 82172891), and the Doctoral Foundation of Xinxiang Medical University (No. XYBSKYZZ202001). S.J. was supported in part by the National Natural Science Foundation of China (No. 82074360) and Young Tai shan Scholars Program of Shandong Province (No. tsqn201909200). The APC was funded by the Henan National Science Fund for Excellent Young Scholars (No. 212300410067).

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