Fig. 2

PXR prevents L-OHP-mediated tumor cell growth inhibition and induction of apoptosis. a PXR and empty vector control transfectants were identified by RT–PCR and WB in HCT116. Abundant PXR was detected in PXR transfectants but not in empty vector transfectants. β-actin was used as an internal control. b MTS assays were used to examine the effects of PXR on L-OHP-mediated suppression of tumor cell proliferation. Cell viability was evaluated in triplicate. *P < 0.05; **P < 0.01. c The effects of PXR on L-OHP-mediated cell growth were further confirmed using colony-formation assays. The colonies were counted. The error bars indicate the s.d. (n = 3), **P < 0.01. d The effects of PXR on L-OHP-induced cellular apoptosis were detected by propidium iodide flow cytometric assessment of the sub-G1 fraction. The error bars indicate the s.d. (n = 3). e The effects of PXR on L-OHP-induced cellular apoptosis were detected by Annexin V-APC/7-amino-actinomycin D flow cytometry. The error bars indicate the s.d. (n = 3). f PXR knockdown was confirmed by RT–PCR and WB in SW480 cells. β-actin was used as an internal control. g An MTS assay was performed to assess cell proliferation after PXR knockdown and treatment with L-OHP. Cell viability was evaluated in triplicate. *P < 0.05; **P < 0.01. h The effects of PXR knockdown on L-OHP-induced cellular apoptosis were detected by propidium iodide flow cytometric assessment of the sub-G1 fraction. The error bars indicate the s.d. (n = 3). i Effect of PXR knockdown on L-OHP-induced cell apoptosis was detected by Annexin V-APC/7-amino-actinomycin D flow cytometry. The error bars indicate the s.d. (n = 3)