Figure 6.
Downregulation of endogenous kinesin family member 2C (KIF2C)/mitotic centromere‐associated kinesin (MCAK) expression. (a) p53‐dependent repression of endogenous KIF2C/MCAK protein in p53 +/+ and p53 −/– ; HCT116 cells after DNA damage by treatment of various concentration of adriamycin (ADR; 0, 0.1, 0.2, 0.5, 1 and 2 µg/ml). β‐Actin served as a loading control for western blotting analysis. (b,c) p53‐dependent repression of endogenous KIF2C/MCAK transcription and protein in the breast cancer cell line HBC4 (wild‐type p53) after treatment with 1 µg/mL adriamycin. β2‐Microgloblin (β2MG) and β‐actin served as loading controls for reverse transcription–polymerase chain reaction and western blot analyses, respectively. (d) Increased expression of KIF2C/MCAK after p53 siRNA (sip53) treatment in HBC4 cells. The cells were transfected with sip53 and siEGFP or siLuc (negative controls). β‐Actin served as a loading control.