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PI3K和MEK抑制剂抑制选择性激活的巨噬细胞促乳腺癌细胞浸润迁移的研究

陈静琦 曾波航 朱必胜 侯开连

肿瘤防治研究2013,Vol.40Issue(3):221-225,5.
肿瘤防治研究2013,Vol.40Issue(3):221-225,5.DOI:10.3971/j.issn.1000-8578.2013.03.001

PI3K和MEK抑制剂抑制选择性激活的巨噬细胞促乳腺癌细胞浸润迁移的研究

Study on Inhibitors of PI3K/MEK Prevent Alternatively Activated Macrophages from Promoting Breast Cancer Cell Invasion and Migration

陈静琦 1曾波航 1朱必胜 1侯开连1

作者信息

  • 折叠

摘要

Abstract

Objective To interpret new molecular targets for breast cancer therapy and investigated the molecular mechanism of alternatively activaed macrophages (M2)'s promotion in breast cancer invasion and migration. Methods Mononuclear cells were isolated from peripheral blood of normal adults by den-sity gradient centnfugation.and alternatively activated M2 in vitro. Activation of M2 to breast cancer signal molecules was detected by Western blot. The inhibition function of PI3K/ERK inhibitors to (M2) s promotion in breast cancer migration was evaluated by invasion assay and wound assay. Results To simulate breast cancer microenvironment, we co-cultured M2 and breast cancer MDAMB-231 cells. In the co-cultur system,the inhibitors, LY294002 of PI3K,U()126 of MEK, inhibiting (M2)'s activation to breast cancer PI3K/ERK in 6,12 h. The two inhibitors can prevent (M2) from promoting breast cancer invasion and migration. Conclusion The inhibitors of PI3K/MEK prevent M2 from promoting breast cancer invasion and migration. They can be new targets of breast cancer therapy.

关键词

乳腺癌/选择性激活的巨噬细胞/PI3K/ERK/浸润迁移

Key words

Breast cancer/ Alternatively activated macrophages/ PI3K/ERK/Invastion and migration

分类

医药卫生

引用本文复制引用

陈静琦,曾波航,朱必胜,侯开连..PI3K和MEK抑制剂抑制选择性激活的巨噬细胞促乳腺癌细胞浸润迁移的研究[J].肿瘤防治研究,2013,40(3):221-225,5.

基金项目

国家自然科学基金资助项目(81172537) (81172537)

广州市属高校科技计划项目资助课题(08A080) (08A080)

肿瘤防治研究

OA北大核心CSCDCSTPCD

1000-8578

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