Abstract

Abstract Metastasis is the underlying cause of death in the majority of patients with breast cancer who succumb to their disease, but the fundamental mechanisms remain poorly understood. Here we have found a novel candidate of metastasis-associated protein, MAP40, which is highly expressed membrane protein in the metastatic breast cancer cell lines. Using the public microarray datasets, we also found that MAP40 is significantly increased in the basal type of breast tumors compared to the luminal subtype. We undertook the lentivirus-based system to functionally silence MAP40 gene in basal-like breast cancer cell lines. Knockdown of MAP40 results in a significant reduction of cell migration and invasiveness as well as suppression of anchorage-independent growth in basal-like breast cancer cells. Additionally, depletion of MAP40 induces E-cadherin expression, while integrin β1 protein level is suppressed. Together with results from studies in animal models suggest that MAP40 may promote tumor formation and direct metastasis of breast cancer in vivo. Ongoing studies to find interacting partners and downstream genes will allow us to further understand its mechanism in metastasis. This work was supported by a National Research Foundation grant of Korea (2009-0081756) funded by the Korea government. Citation Format: Mijin Kim, Seong-Jin Kim. A novel candidate metastasis-associated protein, MAP40, differentially expressed in highly metastatic breast cancer cells reveals an essential role in tumor metastasis. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr 2002. doi:10.1158/1538-7445.AM2014-2002

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