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作 者:王松[1] 蒋忠军[1] 包铮[1] 胡聂[1] 罗平[1]
机构地区:[1]南华大学附属南华医院甲乳肿瘤外科,湖南衡阳421002
出 处:《中国肿瘤外科杂志》2015年第4期205-208,共4页Chinese Journal of Surgical Oncology
基 金:湖南省教育厅科技项目(14C0997;13C831);湖南省自然科学基金(12JJ9030)
摘 要: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Cas Ki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 102mmol/L的CS细胞增殖抑制率最高,10-5mmol/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Cas Ki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Cas Ki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Cas Ki细胞株、乳腺癌MDA-MB-231细胞株增殖的效应与抑制h PRLr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Cas Ki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。Objective This study was to investigate the relationship between the effects of CS and prolactin-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,eell proliferation rate was detected by MTT assay, the expression of PRLr was detected by using Western blot, the relationship between cell proliferation rate and expression of PRLr was detected by linear correlation statistical analysis. Results 10^2 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 ceils 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 prolaetin-dependent tumor ceils on CasKi cervical cancer,breast cancer MDA-MB-231 cells in vitro,with the relevant of decreased levels intracellular expression of the PRLr.
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