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机构地区:[1]沈阳医学院基础医学院,辽宁沈阳110034 [2]沈阳医学院基础医学院生物化学与分子生物学教研室,辽宁沈阳110034
出 处:《沈阳医学院学报》2017年第6期530-533,共4页Journal of Shenyang Medical College
基 金:沈阳医学院科研基金项目(No.20141004);沈阳医学院大学生科研课题(No.20179002)
摘 要:目的:探讨辛二酰苯胺异羟肟酸(SAHA)是否经由组织蛋白酶B(CTSB)的有效调控诱导人乳腺癌细胞株MDA-MB-231细胞凋亡的发生。方法:采用Western blot及ELISA法检测SAHA、CTSB抑制剂(Cystain C)对乳腺癌细胞中CTSB表达的影响;采用Muse自动分析仪检测SAHA、Cystain C对乳腺癌MDA-MB-231细胞活力及凋亡的影响。结果:Cystatin C对乳腺癌细胞中CTSB的有效抑制浓度为100 ng/ml;Cystain C和SAHA共同作用乳腺癌细胞后,乳腺癌细胞活力及凋亡细胞比率较单独SAHA处理组相比恢复明显,差异均有统计学意义。结论:SAHA对乳腺癌的生长抑制作用需要CTSB的参与。Objective:To clarify the regulation role of cathepsin B(CTSB) in cell apoptosis induced by SAHA in triplenegative breast cancer cell MDA-MB-231. Methods:MDA-MB-231 cells were incubated with SAHA and/or Cystain C,the expression of CTSB was determined by Western blot and ELISA, the cell viability and apoptosis of MDA-MB-231 cells were detected by Muse cell analyzer. Results:The optimal concentration of Cystain C was 100 ng/ml. The cell viability and apoptosis test demonstrated that the combination treatment of Cystatin C and SAHA significantly resumed the inhibitory effect caused by SAHA alone. Conclusion:CTSB plays an important role in apoptosis induced by SAHA in triple-negative breast cancer cell MDA-MB-231.
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