The Emerging Role of CSN6 in Biological Behavior and Cancer Progress

Author:

Mao Zun1,Chen Cheng1,Pei Dong-Sheng1

Affiliation:

1. Laboratory of Clinical and Experimental Pathology, Xuzhou Medical University, 209 Tong-shan Road, Xuzhou 221004, Jiangsu, China

Abstract

Background:The Constitutive Photomorphogenesis 9 (COP9) signalosome (CSN) subunit 6 (CSN6) noticeably acts as a regulator of the degradation of cancer-related proteins, which contributes to cancerogenesis. The aims of this paper are to expound the research advances of CSN6, particularly focusing on roles of CSN6 in the regulation of biological behavior and cancer progress.Methods:Literature from PubMed and Web of Science databases about biological characteristics and application of CSN6 published in recent years was collected to conduct a review.Results:CSN6, not only the non-catalytic Mpr1p and Pad1p N-terminal (MPN) subunit of CSN, but also a relatively independent protein molecule, has received great attention as a regulator of a wide range of developmental processes by taking part in the ubiquitin-proteasome system and signal transduction, as well as regulating genome integrity and DNA damage response. In addition, phosphorylation of CSN6 increases the stability of CSN6, thereby promoting its regulatory capacity. Moreover, CSN6 is overexpressed in many types of cancer compared with normal tissues and is involved in the regulation of several important intracellular pathways, consisting of cell proliferation, migration, invasion, transformation, and tumorigenesis.Conclusion:We mainly present insights into the function and research development of CSN6, hoping that it can help guide the treatment of developmental defects and improve clinical care, especially in the regulation of cancer signaling pathways.

Funder

Science and Technology Department of Jiangsu Province

Jiangsu Provincial Medical Talent

National Natural Science Foundation of China

Publisher

Bentham Science Publishers Ltd.

Subject

Cancer Research,Pharmacology,Molecular Medicine

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