Abstract
Abstract Background: We previously reported that LIX1L (LIX1-like), a gene whose functions are unknown, has an expression pattern exhibiting strong negative correlation with the expression of genes of epithelial-specific functions in the NCI-60 human cancer cell line panel of the US National Cancer Institute (Kohn et al PLoS ONE 9:6, 2014). This observation suggested a possible role in the epithelial-to-mesenchymal transition (EMT) and led to the current investigation. Method]: We examined the correlation of LIX1L with gene expression in the data of the Broad Institute's CCLE cell lines and the cancer genome atlas (TCGA) tissues. We then investigated the functions of LIX1L in breast and colon cancer cell lines. We knocked down LIX1L expression by means of siRNA and overexpressed LIX1L by means of recombinant LIX1L-GFP plasmid. We also generated LIX1L knockout cell lines (LIX1L-KO) using the CRISPR/Cas system. We compared the expression levels of LIX1L with well-known EMT-related genes by Western blot and quantitative PCR. We examined the migration and invasion properties of these cell lines and constructs by means of wound healing assays, and migration and invasion assays. Results: LIX1L expression is correlated with non-epithelial or mesenchymal genes in analyses of the CCLE and TCGA gene expression data. Experiments suggested the surprising result that LIX1L-KO MDA-MB231 cell lines showed higher expression of ZEB1 and increased invasion ability. Conclusion: LIX1L gene expression is positively correlated with the expression of non-epithelial or mesenchymal genes in the NCI-60, CCLE and TCGA databases. Up- or down-regulation of LIX1L however seemed to produce the opposite of the expected phenotypic changes. Our findings suggest that LIX1L may be expressed coordinately with genes that favor epithelial-to-mesenchymal transitions in cancer cells while having a moderating effect on the transition. Citation Format: Mihoko Yamade, Yves Pommier, Kurt W. Kohn. LIX1L, an EMT-correlated gene that behaves as if it inhibits the EMT. [abstract]. In: Proceedings of the 106th Annual Meeting of the American Association for Cancer Research; 2015 Apr 18-22; Philadelphia, PA. Philadelphia (PA): AACR; Cancer Res 2015;75(15 Suppl):Abstract nr 4104. doi:10.1158/1538-7445.AM2015-4104
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