期刊文献+

胃泌素/CCK-B受体环对多种肿瘤细胞生长和凋亡的影响 被引量:5

Effects of gastrin/CCK- B receptor signaling on growth and apoptosis in selected cancer cell lines
下载PDF
导出
摘要 目的探讨胃泌素/CCK-B受体环对肝癌、肺癌和乳腺癌细胞生长和凋亡的影响。方法用免疫细胞化学检测肺癌A549细胞、肝癌Hep G2细胞及乳腺癌MCF-7细胞系中胃泌素和CCK-B受体的表达。再用CCK-B受体拮抗剂丙谷胺(5 mmol/L)处理细胞(实验组),分别用MTT实验、流式细胞仪及分光光度法检测3种癌细胞的生长曲线、细胞凋亡及caspase-3的酶活性,对照组未用丙谷胺处理。结果肝癌Hep G2细胞、肺癌A549细胞和乳腺癌MCF-7细胞中胃泌素和CCK-B受体的表达均为阳性;与对照组比较,实验组细胞的生长被显著抑制,caspase-3酶活性和凋亡细胞百分数显著升高,差异均有统计学意义(P<0.05,P<0.01)。结论胃泌素/CCK-B受体环参与肝癌、肺癌和乳腺癌细胞的生长和凋亡,阻断此环能抑制细胞的生长,促进细胞凋亡。 Objective To investigate the effects of gastrin/CCK- B receptor signaling on cell growth and apoptosis in liver cancer,lung cancer and breast cancer cell lines. Methods Expression of gastrin and CCK- B receptor was detected in hepatocarcinoma Hep G2 cells,lung carcinoma A549 cells and breast cancer MCF- 7 cells by immunocytochemistry. After treatment of 5 mmol / L proglumide( experimental groups),a CCK- B receptor antagonist,the cell growth curve,apoptosis and caspase- 3 activity were detected by MTT assay,flow cytometry and spectrophotometry,respectively. The control groups were not treated with proglumide. Results The liver cancer Hep G2 cells,lung cancer A549 cells and breast cancer MCK- 7 cells showed positive expression for gastrin and CCK- B receptor. After proglumide treatment,cell growth was significantly inhibited,and caspase- 3 activity and percentage of apoptotic cells significantly increased in all of the experimental groups compared with the control groups( P 0. 05 or P 0. 01). Conclusion Gastrin / CCK- B receptor signaling is involved in the cell growth and apoptosis in hepatocarcinoma,lung carcinoma and breast cancer and blocking of the signal pathway can inhibit cell growth and promote apoptosis.
出处 《广东医学》 CAS 北大核心 2016年第3期332-335,共4页 Guangdong Medical Journal
基金 国家自然科学基金资助项目(编号:81260303) 贵州省2011协同创新中心项目(编号:黔教合协同创新中心[2014]06) 贵州省科学技术基金资助项目(编号:黔科合J字[2012]2039号)
关键词 胃泌素 CCK-B受体 肿瘤 细胞生长 细胞凋亡 gastrin CCK-B receptor cancer cell growth apoptosis
  • 相关文献

参考文献4

二级参考文献18

共引文献42

同被引文献31

引证文献5

二级引证文献9

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部