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Int. J. Mol. Sci. 2015, 16(3), 4560-4580;

Roles of Ubiquitination and SUMOylation on Prostate Cancer: Mechanisms and Clinical Implications

Department of Biochemistry and Cancer Biology, Meharry Medical College, Nashville, TN 37208, USA
Author to whom correspondence should be addressed.
Academic Editor: William Chi-Shing Cho
Received: 14 January 2015 / Revised: 9 February 2015 / Accepted: 12 February 2015 / Published: 27 February 2015
(This article belongs to the Collection Advances in Molecular Oncology)
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The initiation and progression of human prostate cancer are highly associated with aberrant dysregulations of tumor suppressors and proto-oncogenes. Despite that deletions and mutations of tumor suppressors and aberrant elevations of oncogenes at the genetic level are reported to cause cancers, emerging evidence has revealed that cancer progression is largely regulated by posttranslational modifications (PTMs) and epigenetic alterations. PTMs play critical roles in gene regulation, cellular functions, tissue development, diseases, malignant progression and drug resistance. Recent discoveries demonstrate that ubiquitination and SUMOylation are complicated but highly-regulated PTMs, and make essential contributions to diseases and cancers by regulation of key factors and signaling pathways. Ubiquitination and SUMOylation pathways can be differentially modulated under various stimuli or stresses in order to produce the sustained oncogenic potentials. In this review, we discuss some new insights about molecular mechanisms on ubiquitination and SUMOylation, their associations with diseases, oncogenic impact on prostate cancer (PCa) and clinical implications for PCa treatment. View Full-Text
Keywords: posttranslational modifications; ubiquitination; SUMOylation; prostate cancer posttranslational modifications; ubiquitination; SUMOylation; prostate cancer

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Chen, Z.; Lu, W. Roles of Ubiquitination and SUMOylation on Prostate Cancer: Mechanisms and Clinical Implications. Int. J. Mol. Sci. 2015, 16, 4560-4580.

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