机构地区:[1]浙江中医药大学,310053 [2]海警医院,310023 [3]浙江省嘉兴市第一医院,314001
出 处:《浙江临床医学》2022年第2期171-175,共5页Zhejiang Clinical Medical Journal
摘 要:目的探讨右美托咪定对人乳腺癌SKBR-3细胞株MAPK/JNK/Bcl-2信号通路及癌细胞转移、侵袭的影响。方法人乳腺癌SKBR-3细胞株细胞设SKBR-3细胞组、顺铂组(100.0 μg/mL)、右美托咪定低剂量组(100.0 μg/mL)、右美托咪定高削量组(200.0 μg/mL),各组每孔设6个平行样,培养72 h。培养结束后,使用MTT测定法测定细胞活力,Giemsa溶液染色计算克隆形成教目,伤口愈合测试细胞侵袭能力,流式细胞仪测定细胞凋亡水平,RT-PCR法及western-blot法测细胞MAPK、JNK、Bcl-2基因和蛋白水平。结果与SKBR-3细胞组比较,顺柏组、右美托咪定低/高剂量组的OD值、存活率、克隆形成数目、侵袭距离、MAPK、JNK、Bcl-2 mRNA和蛋白水平均降低(P<0.05),凋亡率升高(P<0.05)。与顺铂组比较,右美托咪定低/高剂量组的OD值、存活率、克隆形成数目、侵袭距离、MAPK、JNK、Bcl-2 mRNA和蛋白水平均升高(P<0.05),凋亡率降低(P<0.05)。与右美托咪定低剂量组比较,右美托咪定高剂量组的OD值、存活率、克隆形成数目、侵袭距离、MAPK、JNK、Bcl-2 mRNA和蛋白水平均降低(P<0.05),凋亡率升高(P<0.05)。结论右美托咪定能明显抑制SKBR-3乳腺癌细胞增殖、转移、侵袭,促进其凋亡,与剂量呈正性相关,其作用机制可能与明显抑制SKBR-3细胞MAPK、JNK、Bcl-2 mRNA和蛋白的表达进而抑制MAPK/JNK/Bcl-2信号通路的激活有关。Objective To investigate the effects of dexmedetomidine on MAPK/JNK/Bcl-2 signaling pathway,metastasis and invasion of human breast cancer SKBR-3 cell line.Methods Human breast cancer SKBR-3 cell line was divided into SKBR-3 cell group,cisplatin group(100.0μg/mL),dexmedetomidine low-dose group(100.0μg/mL),and dexmedetomidine high-dose group(200.0μg/mL),with 6 parallel samples per well in each group for 72 h.When the culture was over,the cell viability was measured by MTT assay,the number of clones formed was calculated by Giemsa solution staining,the cell invasion ability was measured by wound healing,the apoptosis level was measured by flow cytometry,and the cell MAPK,JNK,Bcl-2 gene and protein levels were measured by RT-PCT and western-blot.Results Compared with SKBR-3 cell group,the OD,survival rate,number of clonal formation,invasion distance,MAPK,JNK,Bcl-2 mRNA and protein levels in cisplatin group,dexmedetomidine group and high dose group were significantly decreased,while apoptosis rate were significantly increased(P<0.05).Compared with cisplatin group,the OD,survival rate,number of clonal formation,invasion distance,MAPK,JNK,Bcl-2 mRNA and protein in dexmedetomidine low dose group and high dose group were significantly increased,while apoptosis rate were significantly decreased(P<0.05).Compared with the dexmedetomidine low dose group,the OD,survival rate,number of clonal formation,invasion distance,MAPK,JNK,Bcl-2 mRNA and protein levels in the high dose group were significantly decreased,while the apoptosis rate were increased(P<0.05).Conclusion Dexmedetomidine can significantly inhibit the proliferation,metastasis,invasion of SKBR-3 breast cancer cell,promote its apoptosis,and have positive correlation with dose.Its mechanism may be related to that dexmedetomidine can significantly inhibit the expression level of MAPK,JNK,Bcl-2 mRNA and protein of SKBR-3 cells,and then inhibiting MAPK/JNK/Bcl-2 signaling pathway activation.
关 键 词:右美托咪定 人乳腺癌SKBR-3细胞株 转移 侵袭 MAPK/JNK/Bcl-2信号通路
正在载入数据...
正在载入数据...
正在载入数据...
正在载入数据...
正在载入数据...
正在载入数据...
正在载入数据...