Upregulation of lncRNA CCAT2 predicts poor prognosis in patients with acute myeloid leukemia and is correlated with leukemic cell proliferation.

Increasing data have shown that the dysregulation of long non-coding RNAs (lncRNAs) is associated with a variety of human cancers, including acute myeloid leukemia (AML). Colon cancer-associated transcript-2 (CCAT2) gene encodes an lncRNA CCAT2 whose over-activation was observed in many human solid tumors. However the expression and clinical significance of CCAT2 in AML have not been identified. In the study, we found that CCAT2 expression levels in patients with AML were significantly increased compared with healthy individuals. The patients with highly expressed CCAT2 had higher white blood cells than those patients with low CCAT2. The incidence of FLT3/ITD mutation in the patients with high CCAT2 expression was significantly higher than in those patients with low CCAT2 expression. High CCAT2 expression was correlated with more monosomal karyotype and poor risk stratification. Furthermore, patients with high CCAT2 had significantly shorter overall survival times than those patients with low CCAT2. Univariate and multivariate Cox's analyses indicated a poor prognostic value of high CCAT2 in AML patients. Moreover, in vitro assay revealed that overexpression of CCAT2 promoted KG-1 cell proliferation and induced cell cycle arrest at the S phase, whereas CCAT2 knockdown inhibited proliferation by inducing cell-cycle arrest at the G2/M phase. In conclusion, our study demonstrates for the first time that CCAT2 is highly expressed in AML patients, and it associates with poor prognosis and leukemic cell proliferation.