Inhibitory Effects of Oridonin Combined with Gemcitabine on Pancreatic Cancer SW1990 Cells
Limin Zhou
Abstract
Limin Zhou
Abstract
Objective cancer SW1990 cells in vitro, and the potential mechanisms thereof. Methods The pancreatic cancer SW1990 cells weretreated with vehicle alone and various concentrations(10,20,40,80 and160 μmol/L) of oridonin, followed by 24, 48 and 72 hcell culture. Effects of oridonin on cell proliferation were determined by using a CCK-8 kit. SW1990 cells were treated withoridonin(40 μmol/L) and gemcitabine(20 μmol/L) alone or together for 48 h, and the untreated cells were used as the con-trol. The cell survival rate was detected by CCK-8 assay. Apoptosis induction was assessed by using Annexin V-FITC kit.Semi-quantitative RT-PCR was used to examine the changes of NF-κB mRNA and XIAP mRNA expressions. ResultsOridonin inhibited the growth of pancreatic cancer SW1990 cells in a dose- and time-dependent manner. Compared withthe other groups, the cell survival rate was significantly lower in the combination group(P 0.05). Oridonin combined withgemcitabine induced a higher percentage of apoptosis in pancreatic cancer cells than that of oridonin or gemcitabine alone(P 0.05). Moreover, the expressions of NF-κB and XIAP mRNA in pancreatic carcinoma cells were obviously down-regu-lated in combination group(P 0.05). Conclusion Oridonin can enhance the antitumor effect of gemcitabine on pancreaticcancer in vitro, which may be related to through the down-regulation of NF-κB and its downstream of XIAP, and then induc-ing cell apoptosis in pancreatic cancer.
A significance statement is not available in the OpenAlex record.
A contribution statement is not available in the OpenAlex record.
Method details are not available in the OpenAlex metadata.
Findings are not separately available in the OpenAlex metadata.
Limitations are not available in the OpenAlex metadata.
Application details are not available in the OpenAlex metadata.
Objective cancer SW1990 cells in vitro, and the potential mechanisms thereof. Methods The pancreatic cancer SW1990 cells weretreated with vehicle alone and various concentrations(10,20,40,80 and160 μmol/L) of oridonin, followed by 24, 48 and 72 hcell culture. Effects of oridonin on cell proliferation were determined by using a CCK-8 kit. SW1990 cells were treated withoridonin(40 μmol/L) and gemcitabine(20 μmol/L) alone or together for 48 h, and the untreated cells were used as the con-trol. The cell survival rate was detected by CCK-8 assay. Apoptosis induction was assessed by using Annexin V-FITC kit.Semi-quantitative RT-PCR was used to examine the changes of NF-κB mRNA and XIAP mRNA expressions. ResultsOridonin inhibited the growth of pancreatic cancer SW1990 cells in a dose- and time-dependent manner. Compared withthe other groups, the cell survival rate was significantly lower in the combination group(P 0.05). Oridonin combined withgemcitabine induced a higher percentage of apoptosis in pancreatic cancer cells than that of oridonin or gemcitabine alone(P 0.05). Moreover, the expressions of NF-κB and XIAP mRNA in pancreatic carcinoma cells were obviously down-regu-lated in combination group(P 0.05). Conclusion Oridonin can enhance the antitumor effect of gemcitabine on pancreaticcancer in vitro, which may be related to through the down-regulation of NF-κB and its downstream of XIAP, and then induc-ing cell apoptosis in pancreatic cancer.
Key concepts: Gemcitabine, XIAP, Pancreatic cancer, Apoptosis, Annexin, In vitro, Cancer research, Cell culture