中国肿瘤外科杂志
中國腫瘤外科雜誌
중국종류외과잡지
CHINESE MEDICAL DIGEST SURGERY
2015年
4期
205-208
,共4页
王松%蒋忠军%包铮%胡聂%罗平
王鬆%蔣忠軍%包錚%鬍聶%囉平
왕송%장충군%포쟁%호섭%라평
半胱胺%催乳素%催乳素受体%宫颈癌%乳腺癌%结肠癌%直线相关分析
半胱胺%催乳素%催乳素受體%宮頸癌%乳腺癌%結腸癌%直線相關分析
반광알%최유소%최유소수체%궁경암%유선암%결장암%직선상관분석
Cysteamine%prolactin%prolactin receptor%cervical cancer%breast cancer%colon %cancer%Linear correlation analysis
目的：通过半胱胺( Cysteamine,CS)对体外催乳素依赖性肿瘤细胞的影响与催乳素受体( prolactin receptor,PRLr)的相关性研究,来探讨CS抑制催乳素依赖性肿瘤的机制。方法以人宫颈癌CasKi细胞株、乳腺癌MDA-MB-231细胞株、结肠癌SW480细胞株为研究对象,MTT法检测CS对细胞增殖的影响,Western Blot检测CS对各细胞中PRLr的表达量影响,直线相关统计分析CS的细胞增殖抑制率与PRLr表达量的关系。结果102 mmol/L的CS细胞增殖抑制率最高,10-5 mmol/L以下无增殖抑制作用,抑制效益呈剂量依赖性；CS对催乳素依赖性肿瘤细胞的抑制作用在24h时细胞抑制率最高,且对宫颈癌CasKi细胞株增殖抑制作用最大,乳腺癌MDA-MB-231细胞株次之,结肠癌SW480细胞株最低。PRLr在宫颈癌CasKi细胞株中表达量最高,乳腺癌MDA-MB-231细胞株次之,结肠癌SW480细胞株最低；CS抑制宫颈癌CasKi细胞株、乳腺癌MDA-MB-231细胞株增殖的效应与抑制hPRLr的表达成负相关。结论低浓度CS能在体外抑制催乳素依赖性肿瘤宫颈癌CasKi细胞、乳腺癌MDA-MB-231细胞的增殖,可能与降低细胞内的PRLr表达水平有关。
目的：通過半胱胺( Cysteamine,CS)對體外催乳素依賴性腫瘤細胞的影響與催乳素受體( prolactin receptor,PRLr)的相關性研究,來探討CS抑製催乳素依賴性腫瘤的機製。方法以人宮頸癌CasKi細胞株、乳腺癌MDA-MB-231細胞株、結腸癌SW480細胞株為研究對象,MTT法檢測CS對細胞增殖的影響,Western Blot檢測CS對各細胞中PRLr的錶達量影響,直線相關統計分析CS的細胞增殖抑製率與PRLr錶達量的關繫。結果102 mmol/L的CS細胞增殖抑製率最高,10-5 mmol/L以下無增殖抑製作用,抑製效益呈劑量依賴性；CS對催乳素依賴性腫瘤細胞的抑製作用在24h時細胞抑製率最高,且對宮頸癌CasKi細胞株增殖抑製作用最大,乳腺癌MDA-MB-231細胞株次之,結腸癌SW480細胞株最低。PRLr在宮頸癌CasKi細胞株中錶達量最高,乳腺癌MDA-MB-231細胞株次之,結腸癌SW480細胞株最低；CS抑製宮頸癌CasKi細胞株、乳腺癌MDA-MB-231細胞株增殖的效應與抑製hPRLr的錶達成負相關。結論低濃度CS能在體外抑製催乳素依賴性腫瘤宮頸癌CasKi細胞、乳腺癌MDA-MB-231細胞的增殖,可能與降低細胞內的PRLr錶達水平有關。
목적：통과반광알( Cysteamine,CS)대체외최유소의뢰성종류세포적영향여최유소수체( prolactin receptor,PRLr)적상관성연구,래탐토CS억제최유소의뢰성종류적궤제。방법이인궁경암CasKi세포주、유선암MDA-MB-231세포주、결장암SW480세포주위연구대상,MTT법검측CS대세포증식적영향,Western Blot검측CS대각세포중PRLr적표체량영향,직선상관통계분석CS적세포증식억제솔여PRLr표체량적관계。결과102 mmol/L적CS세포증식억제솔최고,10-5 mmol/L이하무증식억제작용,억제효익정제량의뢰성；CS대최유소의뢰성종류세포적억제작용재24h시세포억제솔최고,차대궁경암CasKi세포주증식억제작용최대,유선암MDA-MB-231세포주차지,결장암SW480세포주최저。PRLr재궁경암CasKi세포주중표체량최고,유선암MDA-MB-231세포주차지,결장암SW480세포주최저；CS억제궁경암CasKi세포주、유선암MDA-MB-231세포주증식적효응여억제hPRLr적표체성부상관。결론저농도CS능재체외억제최유소의뢰성종류궁경암CasKi세포、유선암MDA-MB-231세포적증식,가능여강저세포내적PRLr표체수평유관。
Objective This study was to investigate the relationship between the effects of CS and prolac-tin-dependent tumor cells in vitro and PRLr,so as to explore inhibition mechanism of CS on prolactin-dependent tumors. Methods Cervical cancer CasKi cells、breast cancer MDA-MB-231 cells and colon cancer SW480 cells were treated with different concentrations of CS,cell proliferation rate was detected by MTT assay,the ex-pression of PRLr was detected by using Western blot,the relationship between cell proliferation rate and expres-sion of PRLr was detected by linear correlation statistical analysis. Results 102 mmol/L CS had highest rate of cell proliferation,but 10 -5 mmol/L and lower had not,it showed a dose-dependent inhibition efficiency;the cell inhibition rates of CS in 24 h to prolactin-dependent tumor cells were the highest,largest on cervical cancer cell, followed on breast cancer,minimum on colon cancer,the same as the expression of PRLr. The cell proliferation inhibition of cervical cancer,breast cancer and the expression of PRLr had a negative correlation. Conclusions The low concentration CS could inhibit prolactin-dependent tumor cells on CasKi cervical cancer,breast cancer MDA-MB-231 cells in vitro,with the relevant of decreased levels intracellular expression of the PRLr.
