The interaction between lncRNA SNHG1 and miR-140 in regulating growth and tumorigenesis via TLR4/NF-κB pathway in cholangiocarcinoma.

Cholangiocarcinoma (CCA) is the second most common primary hepatobiliary carcinoma. The long non-coding RNA (lncRNA) small nucleolar RNA host gene 1 (SNHG1) has been reported to contribute to the progression of multiple cancers. Nonetheless, the functions and hidden mechanism of SNHG1 remain unclear in CCA. Herein, the SNHG1 levels were boosted in CCA cell lines, and knockdown of SNHG1 repressed CCA cell proliferation and invasion in vitro. The data also demonstrated that miR-140 could act as a target of SNHG1 in CCA, and inhibited CCA cell proliferation and invasion, whereas the inhibition effects were relieved by overexpression of SNHG1. In addition, Toll-like receptor 4 (TLR4), a NF-κB-activating signal, was identified to be a target of miR-140. And SNHG1, as a competing endogenous RNA (ceRNA) for miR140, enhanced TLR4 expression and activated NF-κB signaling, thereby regulating growth and tumorigenesis in CCA. Animal experiments further confirmed this conclusion. Collectively, these findings not only uncovered a key role of SNHG1/miR-140/TLR4/NF-κB signaling axis in CCA tumorigenesis and progression, but also denoted the probable utilization of SNHG1 as a therapeutic target for CCA.