Wnt2 complements Wnt/β-catenin signaling in colorectal cancer

• DOI: 10.18632/oncotarget.6133
• Publication Date: 2015-10-19T01:26:06Z
• Authors: Youn-Sang Jung; Sohee Jun; Sun Hye Lee; Amrish Sharma; Jae-Il Park
• Keywords: 0301 basic medicine; Time Factors; Transcription, Genetic; Polycomb Repressive Complex 2; Adenocarcinoma; DNA Methylation; HCT116 Cells; Transfection; Methylation; Epigenesis, Genetic; 3. Good health; Gene Expression Regulation, Neoplastic; Histones; Autocrine Communication; 03 medical and health sciences; Humans; Enhancer of Zeste Homolog 2 Protein; RNA Interference; Intestinal Mucosa; Colorectal Neoplasms; Promoter Regions, Genetic; Wnt Signaling Pathway; Cell Proliferation

Wnt2 is implicated in various human cancers. However, it remains unknown how upregulated cancer and contributes to tumorigenesis. Here we found that highly expressed colorectal (CRC) cells. In addition co-expression of with Wnt/β-catenin target genes CRC, knockdown or knockout significantly downregulates gene expression CRC Importantly, depletion ablation endogenous inhibits cell proliferation. Similarly, neutralizing secreted reduces Wnt suppresses Conversely, increases proliferation intestinal epithelial Intriguingly, WNT2 transcriptionally silenced by EZH2-mediated H3K27me3 histone modification non-CRC cells, de-repressed the loss PRC2's promoter occupancy Our results reveal unexpected roles complementing signaling for