@article{Ling01092013,
author = {Ling, Hui and Spizzo, Riccardo and Atlasi, Yaser and Nicoloso, Milena and Shimizu, Masayoshi and Redis, Roxana S. and Nishida, Naohiro and Gafà, Roberta and Song, Jian and Guo, Zhiyi and Ivan, Cristina and Barbarotto, Elisa and De Vries, Ingrid and Zhang, Xinna and Ferracin, Manuela and Churchman, Mike and van Galen, Janneke F. and Beverloo, Berna H. and Shariati, Maryam and Haderk, Franziska and Estecio, Marcos R. and Garcia-Manero, Guillermo and Patijn, Gijs A. and Gotley, David C. and Bhardwaj, Vikas and Shureiqi, Imad and Sen, Subrata and Multani, Asha S. and Welsh, James and Yamamoto, Ken and Taniguchi, Itsuki and Song, Min-Ae and Gallinger, Steven and Casey, Graham and Thibodeau, Stephen N. and Le Marchand, Loïc and Tiirikainen, Maarit and Mani, Sendurai A. and Zhang, Wei and Davuluri, Ramana V. and Mimori, Koshi and Mori, Masaki and Sieuwerts, Anieta M. and Martens, John W.M. and Tomlinson, Ian and Negrini, Massimo and Berindan-Neagoe, Ioana and Foekens, John A. and Hamilton, Stanley R. and Lanza, Giovanni and Kopetz, Scott and Fodde, Riccardo and Calin, George A.}, 
title = {CCAT2, a novel noncoding RNA mapping to 8q24, underlies metastatic progression and chromosomal instability in colon cancer},
volume = {23}, 
number = {9}, 
pages = {1446-1461}, 
year = {2013}, 
doi = {10.1101/gr.152942.112}, 
abstract ={The functional roles of SNPs within the 8q24 gene desert in the cancer phenotype are not yet well understood. Here, we report that CCAT2, a novel long noncoding RNA transcript (lncRNA) encompassing the rs6983267 SNP, is highly overexpressed in microsatellite-stable colorectal cancer and promotes tumor growth, metastasis, and chromosomal instability. We demonstrate that MYC, miR–17–5p, and miR–20a are up-regulated by CCAT2 through TCF7L2-mediated transcriptional regulation. We further identify the physical interaction between CCAT2 and TCF7L2 resulting in an enhancement of WNT signaling activity. We show that CCAT2 is itself a WNT downstream target, which suggests the existence of a feedback loop. Finally, we demonstrate that the SNP status affects CCAT2 expression and the risk allele G produces more CCAT2 transcript. Our results support a new mechanism of MYC and WNT regulation by the novel lncRNA CCAT2 in colorectal cancer pathogenesis, and provide an alternative explanation of the SNP-conferred cancer risk.}, 
URL = {http://genome.cshlp.org/content/23/9/1446.abstract}, 
eprint = {http://genome.cshlp.org/content/23/9/1446.full.pdf+html}, 
journal = {Genome Research} 
}