Abstract
Abstract Invasion and metastasis are complex processes that are primarily responsible for most cancer-related deaths throughout the world, and which involve several different biological processes. The IMPs (IGF2 mRNA-binding Proteins) are a family of oncofoetal proteins that includes the members IMP1, p62/IMP2, and IMP3. These proteins are expressed during embryogenesis, and after birth their expression is lost in almost all tissues. Re-expression of IMPs is however evident in a number of adult malignancies. Indeed, p62/IMP2 was initially identified as an autoantigen with serum from a patient with hepatocellular carcinoma (HCC). p62/IMP2 is therefore a potential biomarker for the early diagnosis of HCC as well as of other cancers. Nonetheless, its function is largely unknown. To begin to understand the biology of p62/IMP2, we evaluated its expression in breast cancer by carrying out immunohistochemical analysis of 118 human sections from normal and malignant breast tissue samples. We observed a statistically significant (p<0.05) overexpression of p62/IMP2 in human breast tumors (72/104, 69%), compared with normal human breast tissue (2/14, 14%). Transfection of human p62/IMP2 cDNA into human MDA-MB-231 breast cancer cells (which lack p62/IMP2expression) produced clones with stable positive and negative p62/IMP2 expression, a result confirmed by both western blotting and immunofluorescence analysis. Analysis of the transfected clones, using a wound healing assay, showed that p62/IMP2 overexpression can significantly enhance MDA-MB-231 cell migration. Our results show that p62/IMP2 is expressed in human breast cancers, and that its expression can increase cell migration, which suggests is may promote the invasive behavior of breast cancers. Citation Format: Yang Li, Bo Peng, Ningjing Lei, Giulio Francia, Jianying Zhang. Overexpression of p62/IMP2 in breast cancer promotes cell migration. [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 4922. doi:10.1158/1538-7445.AM2013-4922
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