Cholangiocarcinoma (CCA) is the most usual malignancy of biliary tract, possessing a relatively low overall survival rate due to limited treatment options. Recently, long non-coding RNAs (lncRNAs) have been testified to have marked regulatory impacts on human cancers. The purpose of this paper is to explore the potent regulation mechanism of LINC01061 involved in CCA. Firstly, it was observed that LINC01061 expression was heightened in CCA cell lines, whose knockdown suppressed cell proliferation, induced cell apoptosis and restrained cell migration. Besides, LINC01061 existing in the cytoplasm of CCA cells interacted with miR-612. Moreover, subsequent experiments affirmed that LINC01061 regulated SEMA4D expression by acting as a competing endogenous RNA (ceRNA) of miR-612. At last, rescue assays validated that SEMA4D overexpression restored the repression caused by LINC01061 silence on the biological activities of CCA containing cell proliferation, apoptosis and migration. To sum up, our present exploration demonstrated that LINC01061 sponges miR-612 so as to upregulate SEMA4D expression for the progression of CCA, suggesting an optional promising and effective target for the therapy of patients with CCA.
Keywords: Cholangiocarcinoma (CCA); LINC01061; SEMA4D; miR-612.
Copyright © 2019 Elsevier Inc. All rights reserved.