Copyright
©The Author(s) 2017.
World J Gastroenterol. Jun 14, 2017; 23(22): 4007-4015
Published online Jun 14, 2017. doi: 10.3748/wjg.v23.i22.4007
Published online Jun 14, 2017. doi: 10.3748/wjg.v23.i22.4007
Figure 2 PLK-inhibitor BI6727 induces apoptotis in Mz-Ch-1 cells.
Cleavage of PARP in Mz-Ch-1 treated with the PLK-inhibitor BI6727 (200 nmol/L for 24 h), the cytostatic drug cisplatin (1 mmol/L for 24 h) or both components was assessed by Western blot analysis (A) and densitometric quantification followed by normalization to loading control actin and shown as foldchange compared to vehicle-treated cells (B, mean ± SEM, n = 2). PLK: Polo-like kinase; PARP: Poly(ADP-ribose) polymerase 1.
- Citation: Sydor S, Jafoui S, Wingerter L, Swoboda S, Mertens JC, Gerken G, Canbay A, Paul A, Fingas CD. Bcl-2 degradation is an additional pro-apoptotic effect of polo-like kinase inhibition in cholangiocarcinoma cells. World J Gastroenterol 2017; 23(22): 4007-4015
- URL: https://www.wjgnet.com/1007-9327/full/v23/i22/4007.htm
- DOI: https://dx.doi.org/10.3748/wjg.v23.i22.4007