Long noncoding RNA FAL1 promotes proliferation and inhibits apoptosis of human colon cancer cells.

Aberrant expression of long non-coding RNAs (lncRNAs) has been associated with a variety of malignancies including colon cancer. In this study, we aimed to characterize the biological mechanisms of focally amplified lncRNA on chromosome 1 (FAL1) in colon cancers. Here, our results indicate that FAL1 expression was remarkably up-regulated in colon tumor tissues as compared to corresponding tumor-adjacent normal tissues. Importantly, the cumulative survival rate of patients with high levels of FAL1 in tumor tissues was considerably lower than those with low FAL1 levels in tumor tissues. Cox regression analysis showed that lncRNA FAL1 could act as an independent prognostic factor in CRC. Knockdown of FAL1 in HT29 cells attenuated cell proliferation and stimulated cell apoptosis. In contrast, overmetastasis-related molecules Bcl-2, TGF-β1, p65, and PCNA at the mRNA and protein levels. Mechanistically, FAL1 was found to interact with STAT3 at 200 to 400 bp and promote phosphorylation of STAT3. In addition, we found that knockdown of STAT3 in HT29 cells abolished the effects of FAL1 on cell proliferation as well as the expression of TGF-β1 and Bcl-2. Based on these findings, we concluded that FAL1 might be a potential oncogene for the progression of colon cancer.