The Pathophysiological Factors of Type 2 Diabetes Induce Centrosome Amplification Via SKA1

Abstract: In the present study， we investigated the molecular mechanism of diabetes-associated cell centrosome amplification and proved that the pathophysiological factors of type 2 diabetes induced the centrosome amplification via spindle and kinetochore associated complex protein 1(SKA1). Firstly， cells were treated with the pathophysiological factors of type 2 diabetes (high glucose， high insulin， and high free fatty ) and centrosome amplification was detected by immunofluorescence. Secondly， the expression of SKA1 was detected by Western blot. Finally， the effect on the centrosome amplification after interference with SKA1 was detected by immunofluorescence. The results showed that high glucose， high insulin， high palmitic acid significantly induced the centrosome amplification in HCT116， MCF-7 and Hela cell， the centrosome amplification rate of the treatment group was significantly higher than the control group (P<0.01). The expression of SKA1 protein in the diabetic disease treatment group was significantly increased (P<0.01)， and the expression of SKA1 protein in SKA1 siRNA group was significantly lower than that in the three-factor treatment group (P<0.01). The centrosome amplification rate of SKA1 siRNA group was significantly lower than which of the three-factor treatment group (P<0.01). This study demonstrates that the pathophysiological factors of type 2 diabetes induce cell centrosome amplification via SKA1 in HCT116， MCF-7， and Hela cell.

CSTR: 32200.14.cjcb.2019.01.0010