Abstract
<div>Abstract<p>The <i>Protocadherin 10</i> (<i>PCDH10</i>) is inactivated often by promoter hypermethylation in various human tumors, but its possible functional role as a tumor suppressor gene is not established. In this study, we identify <i>PCDH10</i> as a novel Wnt pathway regulatory element in endometrioid endometrial carcinoma (EEC). <i>PCDH10</i> was downregulated in EEC tumor cells by aberrant methylation of its promoter. Restoring <i>PCDH10</i> levels suppressed cell growth and triggered apoptosis in EEC cells and tumor xenografts. Gene expression profiling revealed as part of the transcriptomic changes induced by <i>PCDH10</i> a reduction in levels of <i>MALAT1</i>, a long noncoding RNA, that mediated tumor suppression functions of <i>PCDH10</i> in EEC cells. We found that <i>MALAT1</i> transcription was regulated by Wnt/β-catenin signaling via TCF promoter binding and <i>PCDH10</i> decreased <i>MALAT1</i> by modulating this pathway. Clinically, <i>MALAT1</i> expression was associated with multiple parameters in patients with EEC. Taken together, our findings establish a novel PCDH10–Wnt/β-catenin–MALAT1 regulatory axis that contributes to EEC development. <i>Cancer Res; 74(18); 5103–17. ©2014 AACR</i>.</p></div>
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