Abstract
Down Syndrome Cell Adhesion Molecule antisense1 (DSCAM-AS1), a novel long non-coding RNA (lncRNA), reportedly contributes to the development and progression of several cancers. There is a lack of information on its biological role and regulatory mechanism with respect to colorectal cancer (CRC). Here, we discovered that the expression of DSCAM-AS1 exhibited a significant upregulation in CRC tissues and cell lines in comparison with the corresponding control. Increased DSCAM-AS1 expression was associated with poor prognosis for those diagnosed with CRC. Loss-of function assay illustrated that knockdown of DSCAM-AS1 resulted in significant inhibition of cell proliferation, invasion and migration in vitro, and impaired tumor growth in vivo. MicroRNA-384(miR-384) was directly targeted by DSCAM-AS1 in CRC cells, and repression of DSCAM-AS1 inhibited the expression of AKT3, a known target of miR-384 in CRC. In addition, repression of miR-384 or overexpression of AKT3 could partially rescue the inhibitory effect of DSCAM-AS1 knockdown on CRC progression. In summary, DSCAM-AS1 exerted an oncogenic role in CRC by functioning as a competing endogenous RNA of miR-384 to bring about regulation of AKT3 expression. These results implied that DSCAM-AS1 might be a novel therapeutic target for patients suffering from CRC.