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. Author manuscript; available in PMC: 2010 Nov 1.
Published in final edited form as: Mol Carcinog. 2009 Nov;48(11):1018–1029. doi: 10.1002/mc.20553

Figure 4.

Figure 4

Diallyl trisulfide (DATS)-induced mitotic arrest was partially but markedly reversed by knockdown of checkpoint kinase 1 (Chk1) protein. Immunoblotting for total Chk1 and Ser317 phosphorylated Chk1 using lysates from (A) LNCaP and (B) HCT-116 cells treated with DMSO (control) or the indicated concentrations of DATS for 4, 8, and 16 h. Immunoblotting for total Chk1, APC/C substrates (cyclinB1 and securin), and Ser10 phosphorylated histone H3 (a marker of mitotic cells) using lysates from (C) LNCaP and (D) HCT-116 cells transiently transfected with a non-specific siRNA or Chk1-targeted siRNA and treated for 8 h with either DMSO (control) or 40 μM DATS. The blots were stripped and re-probed with anti-actin antibody to ensure equal protein loading. Numbers on top of the band, change in protein level relative to corresponding DMSO-treated control (panels A and B) and DMSO-treated non-specific siRNA transfected cells (panels C and D). Similar results were observed in replicate experiments.