Abstract 3869: MicroRNA-200b blocks breast cancer lung metastasis in an orthotopic mouse mammary xenograft tumor model.

Abstract

Abstract Triple negative, or basal-like, breast cancer is a highly invasive and metastatic form of breast cancer, and is difficult to treat due to the lack of target therapies. Epithelial to mesenchymal transition (EMT) refers to a developmental program that converts epithelial cells to mesenchymal cells, therefore enabling cells to migrate and invade. EMT is tightly controlled during development, and recent studies showed that EMT is often reactivated in cancer and plays an important role in cancer invasion and metastasis, and that EMT can also be regulated by microRNAs. MicroRNAs (miRs) are a large family of small non-coding RNAs that negatively regulate protein-coding gene expression posttranscriptionally. Although the miR-200 family members have been shown to be able to inhibit EMT, their effects on cancer metastasis continue to be controversial. We aim to investigate the effect of miR-200b on triple negative breast cancer lung metastasis and the underlying mechanism. It was found that stably expressing miR-200b in MDA-MB-231 cells blocked lung metastasis in an orthotopic mouse mammary xenograft tumor model. In vitro studies showed that stably expressing miR-200b significantly reduced triple negative breast cancer cell proliferation, migration, and invasion. Furthermore, stably expressing miR-200b also decreased tumor growth and angiogenesis in the orthotopic mouse mammary xenograft tumors. These findings suggest that miR-200b blocks breast cancer lung metastasis through its strong inhibitory effect on multiple-steps including proliferation, migration, invasion and angiogenesis. Citation Format: Brock Humphries, Zhishan Wang, Chengfeng Yang. MicroRNA-200b blocks breast cancer lung metastasis in an orthotopic mouse mammary xenograft tumor model. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 3869. doi:10.1158/1538-7445.AM2013-3869