Astrin: A Key Player in Mitosis and Cancer.

Zhenguang Ying,Ou Sha,Wei Li,Weipeng Jiang,Xia Wang,Jing Yang,Chunman Li,Zeyao Zhu

doi:10.3389/fcell.2020.00866

Abstract

Astrin, which is a spindle-associated protein, was found to be closely related to mitotic spindle formation and maintenance. It interacts with other spindle-related proteins to play a key role in maintaining the attachment of the kinetochore-microtubule and integrity of centrosomes and promoting the centriole duplication. In addition, Astrin was quite recently found to be abnormally highly expressed in a variety of cancers. Astrin promotes the development of cancer by participating in various molecular pathways and is considered as a potential prognostic and survival predictor.

Highlights

Cell division represents the most important life activity of cells and it forms the basis of growth, reproduction, and genetic inheritance of living organisms
Normal mitosis requires the formation of the correct bipolar spindle at metaphase, with microtubules (MTs) from both poles attached to kinetochores (KTs) of the sister chromosomes
Astrin, which forms a complex with small kinetochore associated protein (SKAP) and other partners that include MYC binding protein (MYCBP) and dynein light chain (LC8), play key roles in stabilizing KT-MT attachment (Schmidt et al, 2010; Dunsch et al, 2011; Kern et al, 2017)

Summary

Introduction

Cell division represents the most important life activity of cells and it forms the basis of growth, reproduction, and genetic inheritance of living organisms. Astrin Plays a Key Role as a “Lock” to Strengthen Stability of End-on KT-MT Attachments In KT-MT attachment, spindle MTs attach end-on to KTs, a number of conserved protein complexes on chromosomes. Astrin, which forms a complex with small kinetochore associated protein (SKAP) and other partners that include MYC binding protein (MYCBP) and dynein light chain (LC8), play key roles in stabilizing KT-MT attachment (Schmidt et al, 2010; Dunsch et al, 2011; Kern et al, 2017).

Results

Conclusion