RT Journal
A1 Ling, Hui
A1 Spizzo, Riccardo
A1 Atlasi, Yaser
A1 Nicoloso, Milena
A1 Shimizu, Masayoshi
A1 Redis, Roxana S.
A1 Nishida, Naohiro
A1 Gafà, Roberta
A1 Song, Jian
A1 Guo, Zhiyi
A1 Ivan, Cristina
A1 Barbarotto, Elisa
A1 De Vries, Ingrid
A1 Zhang, Xinna
A1 Ferracin, Manuela
A1 Churchman, Mike
A1 van Galen, Janneke F.
A1 Beverloo, Berna H.
A1 Shariati, Maryam
A1 Haderk, Franziska
A1 Estecio, Marcos R.
A1 Garcia-Manero, Guillermo
A1 Patijn, Gijs A.
A1 Gotley, David C.
A1 Bhardwaj, Vikas
A1 Shureiqi, Imad
A1 Sen, Subrata
A1 Multani, Asha S.
A1 Welsh, James
A1 Yamamoto, Ken
A1 Taniguchi, Itsuki
A1 Song, Min-Ae
A1 Gallinger, Steven
A1 Casey, Graham
A1 Thibodeau, Stephen N.
A1 Le Marchand, Loïc
A1 Tiirikainen, Maarit
A1 Mani, Sendurai A.
A1 Zhang, Wei
A1 Davuluri, Ramana V.
A1 Mimori, Koshi
A1 Mori, Masaki
A1 Sieuwerts, Anieta M.
A1 Martens, John W.M.
A1 Tomlinson, Ian
A1 Negrini, Massimo
A1 Berindan-Neagoe, Ioana
A1 Foekens, John A.
A1 Hamilton, Stanley R.
A1 Lanza, Giovanni
A1 Kopetz, Scott
A1 Fodde, Riccardo
A1 Calin, George A.
T1 CCAT2, a novel noncoding RNA mapping to 8q24, underlies metastatic progression and chromosomal instability in colon cancer
JF Genome Research 
JO Genome Research 
YR 2013 
FD September 01 
VO 23 
IS 9 
SP 1446 
OP 1461 
DO 10.1101/gr.152942.112 
UL http://genome.cshlp.org/content/23/9/1446.abstract 
AB 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.