Open AccessThe Interaction Between lncRNA SNHG1 and miR-140 in Regulating Growth and Tumorigenesis via the TLR4/NF-κB Pathway in Cholangiocarcinoma
Author(s) -
Zhen Li,
Xin Li,
Xiao Jing Du,
Henghui Zhang,
Zhengyang Wu,
Kewei Ren,
Xinwei Han
Publication year - 2019
Publication title -
oncology research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.267
H-Index - 57
eISSN - 1555-3906
pISSN - 0965-0407
DOI - 10.3727/096504018x15420741307616
Subject(s) - carcinogenesis , biology , gene knockdown , long non coding rna , competing endogenous rna , cancer research , microrna , signal transduction , circular rna , microbiology and biotechnology , rna , gene , genetics
Cholangiocarcinoma (CCA) is the second most common primary hepatobiliary carcinoma. The long noncoding 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. In this study, 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), an NF-κB-activating signal, was identified to be a target of miR-140. SNHG1, as a competing endogenous RNA (ceRNA) for miR-140, 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.