2010Zhongguo aizheng zazhiRequires access

Expression of XIAP in pancreatic carcinoma cell line BxPC-3 induced by gemcitabine

Honglin Wang

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Abstract

Background and purpose:x-linked inhibitor of apoptosis (XIAP) is one of the crucial kinds of inhibitor of apoptosis protiens (IAPs) which belongs to an apoptosis-supressing factor family. It has been found that XIAP is significantly expressed in many kinds of tumor cells, and there is a correlation between XIAP expression level and chemoresistance. We aimed to study the relationship between chemoresistance and the expression of XIAP induced by gemcitabine (GEM) in pancreatic carcinoma cell line BxPC-3. Methods:The pancreatic carcinoma cell line BxPC-3 was incubated in DMEM, and the cells were treated with 3.10 μg/mL GEM for different sections (0, 24, 36, 48 and 72 h, 0 h was the contral group). Then changes of the cell cycle and apoptosis index were evaluated by flow cytometry, mRNA transcription and expression of XIAP were also examined by RT-PCR and Western blot. Results:In control group the apoptosis rate was (1.23±1.6)%, while the apoptosis rates were (10.3±1.8)%, (14.2±1.5)%, (18.8±1.7)% and (20.3±2.0)%, respectively, in experimental groups, cell cycle analysis showed that G0-G1 phase arrest was induced by GEM, and there was a significant differences (F=146.24, P0.05). But there was no significant difference in apoptosis rates between the 48 h and 72 h groups (P0.05). We also found that the longer the cells were treated with GEM, the more mRNA transcription and expression of XIAP were detected (F=83.72, F=103.58, P0.05). Between the 24 h group and 36 h group (P0.05), which were different from the 36 h and 48 h groups, 48 h and 72 h groups (P0.05), no significant differences were found in mRNA transcription and expression of XIAP. Conclusion:GEM could obviously inhibit proliferation and induce apoptosis of BxPC-3 cells, and drug sensitivity decreased with prolongation of exposure time. GEM might induce and increase the expression of XIAP, which might influence the apoptosis of the cells later, and the disturbance of apoptosis progression might have contributed to chemoresistance.

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Background and purpose:x-linked inhibitor of apoptosis (XIAP) is one of the crucial kinds of inhibitor of apoptosis protiens (IAPs) which belongs to an apoptosis-supressing factor family. It has been found that XIAP is significantly expressed in many kinds of tumor cells, and there is a correlation between XIAP expression level and chemoresistance. We aimed to study the relationship between chemoresistance and the expression of XIAP induced by gemcitabine (GEM) in pancreatic carcinoma cell line BxPC-3. Methods:The pancreatic carcinoma cell line BxPC-3 was incubated in DMEM, and the cells were treated with 3.10 μg/mL GEM for different sections (0, 24, 36, 48 and 72 h, 0 h was the contral group). Then changes of the cell cycle and apoptosis index were evaluated by flow cytometry, mRNA transcription and expression of XIAP were also examined by RT-PCR and Western blot. Results:In control group the apoptosis rate was (1.23±1.6)%, while the apoptosis rates were (10.3±1.8)%, (14.2±1.5)%, (18.8±1.7)% and (20.3±2.0)%, respectively, in experimental groups, cell cycle analysis showed that G0-G1 phase arrest was induced by GEM, and there was a significant differences (F=146.24, P0.05). But there was no significant difference in apoptosis rates between the 48 h and 72 h groups (P0.05). We also found that the longer the cells were treated with GEM, the more mRNA transcription and expression of XIAP were detected (F=83.72, F=103.58, P0.05). Between the 24 h group and 36 h group (P0.05), which were different from the 36 h and 48 h groups, 48 h and 72 h groups (P0.05), no significant differences were found in mRNA transcription and expression of XIAP. Conclusion:GEM could obviously inhibit proliferation and induce apoptosis of BxPC-3 cells, and drug sensitivity decreased with prolongation of exposure time. GEM might induce and increase the expression of XIAP, which might influence the apoptosis of the cells later, and the disturbance of apoptosis progression might have contributed to chemoresistance.

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Available abstract

Background and purpose:x-linked inhibitor of apoptosis (XIAP) is one of the crucial kinds of inhibitor of apoptosis protiens (IAPs) which belongs to an apoptosis-supressing factor family. It has been found that XIAP is significantly expressed in many kinds of tumor cells, and there is a correlation between XIAP expression level and chemoresistance. We aimed to study the relationship between chemoresistance and the expression of XIAP induced by gemcitabine (GEM) in pancreatic carcinoma cell line BxPC-3. Methods:The pancreatic carcinoma cell line BxPC-3 was incubated in DMEM, and the cells were treated with 3.10 μg/mL GEM for different sections (0, 24, 36, 48 and 72 h, 0 h was the contral group). Then changes of the cell cycle and apoptosis index were evaluated by flow cytometry, mRNA transcription and expression of XIAP were also examined by RT-PCR and Western blot. Results:In control group the apoptosis rate was (1.23±1.6)%, while the apoptosis rates were (10.3±1.8)%, (14.2±1.5)%, (18.8±1.7)% and (20.3±2.0)%, respectively, in experimental groups, cell cycle analysis showed that G0-G1 phase arrest was induced by GEM, and there was a significant differences (F=146.24, P0.05). But there was no significant difference in apoptosis rates between the 48 h and 72 h groups (P0.05). We also found that the longer the cells were treated with GEM, the more mRNA transcription and expression of XIAP were detected (F=83.72, F=103.58, P0.05). Between the 24 h group and 36 h group (P0.05), which were different from the 36 h and 48 h groups, 48 h and 72 h groups (P0.05), no significant differences were found in mRNA transcription and expression of XIAP. Conclusion:GEM could obviously inhibit proliferation and induce apoptosis of BxPC-3 cells, and drug sensitivity decreased with prolongation of exposure time. GEM might induce and increase the expression of XIAP, which might influence the apoptosis of the cells later, and the disturbance of apoptosis progression might have contributed to chemoresistance.

Key concepts: XIAP, Apoptosis, Gemcitabine, Inhibitor of apoptosis, Cell cycle, Flow cytometry, Cancer research, Cell culture

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