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. Author manuscript; available in PMC: 2013 Mar 1.
Published in final edited form as: Int J Cancer. 2011 Apr 25;130(5):1029–1035. doi: 10.1002/ijc.26044

Figure 5. HtrA1 contributes to cell sensitivity to chemotherapy which can be reversed by XIAP expression.

Figure 5

A–B downregulation of HtrA1 confers cell resistance to cisplatin induced apoptosis. Stable clones in SKOV3 and TOV-21G cells expressing non-targeting and HtrA1 shRNA (sh1 and sh2) were seeded at 1000 cells/well in 6-well plates, treated with various concentrations of cisplatin for 24 hours, washed, and then incubated in drug-free medium for 2 weeks. Colonies were stained with Coomassie blue and counted. C over-expression of HtrA1 promotes cisplatin toxicity in ovarian cancer cells. OV202 cells were transfected with plasmids encoding WT HtrA1 and treated with Cisplatin for 24h. Apoptotic cells were counted by typan blue staining. D XIAP expression reverses the cell sensitivity to chemotherapy endowed by HtrA1. OV202 cells were transfected with 1μg plasmids encoding HtrA1 cDNA plus various amounts of plasmids encoding XIAP cDNA. After 24h of transfection, cells were treated with 10 μM cisplatin. Cell apoptosis were evaluated by flow cytometry after PI staining 24 h later. Data are expressed as mean ± s.d. from 3 independent trials performed at least in triplicate. *P < 0.05, **P < 0.01