Abstract 1483: Bmi1 is required for Twist1-mediated breast cancer cell invasion.

Abstract

Abstract Metastasis is the spread of cancer cells from the site of primary tumors to distant organs and the establishment of secondary tumors there. It is a multistep process, and the initial step is cancer cell invasion during which cancer cells move into tissues surrounding the tumor and the vasculature. Transcription factor Twist1 has been identified as a key regulator of metastasis in a murine breast tumor model as suppression of Twist1 expression in metastatic mammary carcinoma cells specifically inhibits their ability to metastasize, and overexpression of Twist1 induces cell motility and promotes an epithelial-mesenchymal transition (EMT). Previous studies have shown that Twist1 works together with polycomb group protein Bmi1 to promote EMT. Here we show that in breast cancer cells, Bmi1 acts downstream of Twist1 to promote the cancer cell invasion. Suppression of Bmi1 in breast cancer cells expressing high level Twist1 reduces cell motility, and ectopic expression of Bmi1 in Twist1-knockdown cells promote cell invasion. The results delineate a novel pathway that leads to cancer cell invasion and metastasis, which may benefit the development of novel therapeutic approaches to treat advanced breast cancer. Citation Format: Yu-Huey Lin, Guihua Jing, Junjun Liu. Bmi1 is required for Twist1-mediated breast cancer cell invasion. [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 1483. doi:10.1158/1538-7445.AM2013-1483 Note: This abstract was not presented at the AACR Annual Meeting 2013 because the presenter was unable to attend.