Long non-coding RNA NEAT1 promotes colorectal cancer progression by competitively binding miR-34a with SIRT1 and enhancing the Wnt/β-catenin signaling pathway

In recent years, accumulating evidence has indicated that long non-coding RNAs (lncRNAs) are powerful factors influencing the progression of multiple malignancies. Although a relationship between the lncRNA NEAT1 (nuclear enriched abundant transcript 1) and colorectal cancer has previously been reported, the functional mechanism underlying the involvement of NEAT1 in colorectal cancer remains unknown. In this study, we report that NEAT1 expression is up-regulated in colorectal cancer tissues, which correlates with advanced clinical features, poor overall survival and disease free survival. Up-regulated NEAT1 promotes cell proliferation and metastasis of colorectal cancer both in vitro and in vivo. Moreover, NEAT1 functions as an oncogene influencing cell viability and invasion in part by serving as a competing endogenous RNA (ceRNAs) modulating miRNA-34a expression, leading to subsequent repression of the miR-34a/SIRT1 axis and activation of the Wnt/β-catenin signaling pathway. Taken together, our study demonstrates that the lncRNA NEAT1 may serve as a prognostic biomarker and a potential therapeutic target in colorectal cancer. •LncRNA NEAT1 was significantly up-regulated in colorectal cancer tissues, and correlated with poor overall survival.•NEAT1 was functioned as an oncogene in cell viability and invasion of colorectal cancer.•NEAT1, serving as a competing endogenous RNA, could modulate miRNA-34a expression in colorectal cancer.•NEAT1 regulates SIRT1 expression by competitively binding miR-34a of colorectal cancer.•NEAT1 promotes CRC malignant progression through Wnt/β-catenin signaling pathway of colorectal cancer.