Abstract
Abstract Lung cancer is the most malignant disease which makes lots of people dead worldwide. More and more evidences showed that cancers might arise from chromosome alteration, including amplification or deletion. Our previous study integrating microarray-based comparative genomic hybridization and affymetrix gene expression profiles identified a potential candidate gene, MAPRE2, in a lung cancer cell line model with different invasion capability. MAPRE2 (Microtubule-associated protein RP/EB family member 2) is usually located on microtubule and interactes with tumor suppress gene APC (adenomatous polyposis coli). MAPRE2 might be involved in microtubule polymerization, cell migration and tumorigenesis of colorectal cancers, but its function is unclear. The purpose of this study is to investigate the effects of MAPRE2 on cancer cell function. The results of real-time PCR and western blotting showed that DNA copy number, RNA and protein level of MAPRE2 were higher in low invasive lung cancer cells than in highly invasive cells. Immunofluorescence assay indicated that the distribution of MAPRE2 protein was predominant in cytoplasm. Furthermore, overexpression of MAPRE2 could inhibit cancer cell proliferation, anchorage- dependent and -independent growth, cell motility, invasion ability in vitro and tumor growth and metastasis in vivo. On the contrary, silencing MAPRE2 enhanced lung cancer cell proliferation and invasion ability. Consider the whole map of MAPRE2-regulated signalling, transcriptomic analysis was performed and the results showed that MAPRE2 could affect 1039 genes (ANOVA, FDR< 0.05) which are dominantly involved in cell cycle and adhesion-related biological signalling, such as MAPK, focal adhesion and tight junction pathways. Our results suggested that MAPRE2 might play a significant role in MAPRE2-mediated pathways to suppress tumorigenesis and metastasis. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 77. doi:1538-7445.AM2012-77
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