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茶氨酸衍生物TClC脂质体对雌激素受体阳性的 乳腺癌细胞生长和迁移的抑制作用
杨美玲,刘真真,刘辉,朱荣芹,李筝,闫春燕,盖静,郑晓慧,孙考祥,吴犇昊,张国营
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(烟台大学药学院分子药理学实验室,烟台大学新型制剂与生物技术药物研究山东省高校协同创新中心,分子药理和药物 评价教育部重点实验室(烟台大学),烟台 264005;烟台市毓璜顶医院药学部,烟台 264001;山东营东颖昊生物科技有限公司,烟台 264670)
摘要:
为研发抗癌新药,使用茶氨酸衍生物茶氯香酰胺TClC制备纳米脂质体(TClC-L),研究TClC-L对雌激素受体阳性的人乳腺癌MCF-7细胞生长和迁移的抑制作用,并深入探究可能的作用机制。分别采用MTT和Transwell chamber实验方法探究各浓度TClC-L对MCF-7细胞的生长和迁移的抑制作用;使用流式细胞术(FCM)检测TClC-L对MCF-7细胞凋亡的影响;应用Western blotting检测MCF-7细胞生长和迁移有关蛋白和酶的表达。实验结果显示,TClC-L对MCF-7细胞生长和迁移有显著的抑制、对癌细胞的凋亡表现促进作用;TClC-L明显下调受体蛋白p-VEGFR2、Met和ER-α、抗凋亡蛋白Bcl-2、Cyclin D1、Akt和NF-?B的表达,上调促凋亡蛋白Bax、Caspase-3、p53和p21的表达。TClC-L作用的分子机制可能与抑制VEGFR/Met/ER-α-Akt/NF-?B信号传导通路有关。本研究显示了TClC-L有潜在的治疗雌激素受体阳性乳腺癌的作用。
关键词:  茶氯香酰胺脂质体  雌激素受体阳性的人乳腺癌  生长和迁移  细胞凋亡  抑制作用机制
DOI:10.13610/j.cnki.1672-352x.20180302.021
基金项目:国家科技部十二五“863”项目(2012AA020206), 十三五国家重点研发计划项目(2017YFB0702600)和山东省自然科学基金项目(ZR2015HM004)共同资助。。
Inhibitory effects of theanine derivative TClC liposome on the growth and migrations of ER-ɑ-positive human breast cancer cells
YANG Meiling,LIU Zhenzhen,LIU Hui,ZHU Rongqin,LI Zheng,YAN Chunyan,GE Jing,ZHENG Xiaohui,SUN Kaoxiang,WU Benhao,ZHANG Guoying
(Laboratory of Molecular Pharmacology, School of Pharmacy, Yantai University, Collaborative Innovation Center of Advanced Drug Delivery System and Biotech Drugs in Universities of Shandong, Key Laboratory of Molecular Pharmacology and Drug Evaluation (Yantai University), Ministry of Education, Yantai University, Yantai 264005;Department of Pharmacy,Yuhuangding Hospital of Yantai, Yantai 264001;Shandong Yingdong Yinghao Biotechnology Inc, Yantai 264670)
Abstract:
The purpose of this study was to investigate the inhibitory effects of a theanine derivative TClC-prepared liposome (TClC-L) on the growth and migrations of human breast cancer MCF-7 cells and its potential mechanism. The assays of MTT and transwell chamber were used to explore the effects of TClC-L on the MCF-7 cell grown and migration, respectively. The flow cytometry(FCM)and Western blot were applied to analyzing the effects of TClC-L on the apoptosis and related protein expressions in MCF-7 cells, respectively. The experimental results indicated that TClC-L inhibited the cell growth and migration and promoted the apoptosis of human breast cancer cells. TClC-L significantly down-regulated the protein expression and/or phosphorylation of Bcl-2, p-VEGFR2, Met, ER-α, Cyclin D1, Akt and NF-?B, while it up-regulated the protein expression of Bax, caspase-3, p53, and p21 in MCF-7 cells. The possible molecular mechanism of the TClC-L action against MCF-7 cells might be connected with the suppression of the signal pathway of VEGFR/Met/ER-α-Akt/NF-?B. TClC-L
Key words:  TClC-L  estrogen receptor-positive breast cancer  growth and migration  apoptosis  mechanisms of inhibition

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