期刊文献+

SCP1对人乳腺癌细胞迁移和增殖的影响及其机制

The Effect of SCP1 and Its Mechanisms on the Migration and Proliferation of Human Breast Cancer Cells
下载PDF
导出
摘要 SCP1是一种膜定位的磷酸酶,可以去磷酸化RNA聚合酶Ⅱ并沉默神经元基因.目的:探讨SCP1对人乳腺癌MDA-MB-231细胞迁移和增殖能力的影响,并研究其机制.方法:荧光定量PCR法检测多种癌细胞中SCP1的表达;体外划痕实验检测SCP1对MDA-MB-231细胞迁移能力的影响;Transwell TM细胞侵袭实验检测SCP1对MDA-MB-231细胞侵袭能力的影响;MTT法检测SCP1对MDA-MB-231细胞增殖能力的影响;Western blot法检测SCP1对细胞信号通路分子p-AKT表达的影响.结果:SCP1多种癌细胞中均有表达;SCP1能抑制MDA-MB-231细胞的迁移及增殖能力;抑制SCP1的表达能显著上调MDA-MB-231细胞p-AKT的表达.结论:SCP1可能通过去磷酸化AKT抑制MDA-MB-231细胞迁移和侵袭. SCP1 as a membrane located phosphatases acts globally to silence neuronal genes and to affect the dephosphorylation of RNA PolⅡ.Objective: To investigate the effect and the relevant molecular mechanisms of SCP1 on the migration and proliferation of human breast cancer MDA-MB-231 cell.Methods: The expression of SCP1 in various cancer cells was measured by qRT-PCR.MTT assay was used to evaluate the proliferation capacity in different MDA-MB-231 breast cancer cells.The effects of SCP1 on the expression of p-AKT in MDA-MB-231 cells were examined by Western blotting.In vitro wound healing assay and Transwell^TM assay were utilized to measure the effects of SCP1 on the migration and invasion capability of MDA-MB-231 cells.Results: Suppressed SCP1 significantly promoted the migration and proliferation of MDA-MB-231 cells.Inhibition of SCP1 did not affect the expression of total AKT,whereas the phosphorylated AKT level was markedly up-regulated.Conclusion: SCP1 could inhibit the migration and proliferation of human breast cancer MDA-MB-231 cell via dephosphorylation of AKT.
作者 张亚柯 隋英丽 王梅月 成翠芹 李光勇 王瑞 李军 ZHANG Ya-ke;SUI Ying-li;WANG Mei-yue;CHENG Cui-qin;LI Guang-yong;WANG Rui;LI Jun(School of Pharmacy, Liaocheng University, Liaocheng 252059,China)
机构地区 聊城大学药学院
出处 《聊城大学学报(自然科学版)》 2019年第4期28-33,共6页 Journal of Liaocheng University:Natural Science Edition
基金 国家自然科学基金青年基金(81402512 31401217) 山东省研究生教育创新计划项目(SDYY14016) 山东省高等学校科研计划项目(J13LK17)资助
关键词 SCP1 MDA-MB-231细胞 AKT 细胞迁移 SCP1 MDA-MB-231 cell AKT cell migration
  • 相关文献

参考文献4

二级参考文献80

共引文献887

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