STYK1/NOK affects cell cycle late mitosis and directly interacts with anaphase-promoting complex activator CDH1. Academic Article uri icon

Overview

abstract

  • The novel oncogene STYK1/NOK plays critical roles in cancer development. However, its regulation during cell division is less defined. In this paper, we show that over-expression of STYK1/NOK caused mitotic arrest and cytokinesis defects. The protein level of STYK/NOK fluctuated during the cell cycle, with a peak at mitosis and a quick reduction upon mitotic exit. The cell cycle-related expression pattern of STYK1/NOK resembled the one of aurora kinases and polo-like kinase 1. Depletion of APC3 led to accumulation of STYK1/NOK and to the G2/M arrest. Co-immunoprecipitation experiment demonstrated the direct interaction of STYK1/NOK with CDH1. Overexpression of CDH1 shortened the half-life of STYK1/NOK. The kinase domain, but not the five D boxes, of STYK1/NOK was responsible for the interaction with CDH1. Altogether, our data demonstrated for the first time that STYK1/NOK could affect cell division, probably by directly targeting key components of APC/C such as CDH1 at late mitosis. Current study may provide a vital mechanistic clue for understanding the roles of STYK1/NOK in mitosis and cytokinesis during STYK1NOK mediated genomic instability and oncogenesis.

publication date

  • December 5, 2022

Identity

PubMed Central ID

  • PMC9732331

Scopus Document Identifier

  • 85143881596

Digital Object Identifier (DOI)

  • 10.1016/j.heliyon.2022.e12058

PubMed ID

  • 36506394

Additional Document Info

volume

  • 8

issue

  • 12