摘要
目的检测ERK蛋白在胰腺癌细胞株产生吉西他滨(GEM)化疗抵抗前后的表达,分析ERK通路在化疗抵抗中的作用。方法通过浓度梯度递增诱导法建立对不同浓度吉西他滨化疗抵抗的胰腺癌细胞株模型;应用免疫组化检测各个化疗抵抗浓度细胞株ERK的表达;使用ERK通路阻断剂和激活剂分别作用于化疗抵抗最低和最高浓度,再检测ERK的表达;运用MTT法检测各因素对细胞耐药的影响,计算IC50值。结果经过吉西他滨化疗诱导后,ERK的表达随着化疗抵抗浓度的增加而升高;ERK通路特异性阻断剂作用于最低及最高浓度的化疗抵抗细胞株后,ERK蛋白的表达降低,细胞的1C50值降低,细胞对化疗药物的敏感性增强;ERK通路激活剂作用后,ERK蛋白的表达增强,细胞的IC50值升高,细胞对化疗药物的敏感性增强。结论 ERK通路参与调控胰腺癌细胞吉西他滨化疗抵抗。
Objective To detect the expression of ERK in the pancreatic cancer cells before and after chemoresistance to gemcitabine（ GEM）, then analyze the role of ERK signaling pathway in chemoresistance. Methods Construct the GEM - resistant pancreatic cancer lines model through the method of concentration gradient increasing by degrees ; Immunocytochemistry were used to investigate the expression of ERK in the pancreatic cancer cells chemoresistence to GEM of every concentration ; After the use of the relative antagonist and agonist, detect the expression of ERK again ; Detect the effect of drugs on pancreatic cancer cell lines and the IC50 of each group by MTT method. Results With the GEM concentration increasing, the expression of ERK increased at the same time. the ERK pathway antagonist made the decreasing expression of ERK,whereas the agonist（EGF） made the increasing expression of ERK and IC50. Conclusion ERK signaling pathway may involve the regulation of chemoresistance to GEM in pancreatic cancer cell lines.
出处
《中国医学创新》
CAS
2010年第2期74-75,共2页
Medical Innovation of China
关键词
丝裂原活化蛋白激酶
胰腺肿瘤
化疗抵抗
Mitogen -activated protein kinase
Pancreatic cancer
Chemotherapy resistance
