@Article{096504018X15420741307616,
AUTHOR = {Zhen Li,
 Xin Li,
 Xiao Du, Henghui Zhang, Zhengyang Wu, Kewei Ren, Xinwei Han},
TITLE = {The Interaction Between lncRNA SNHG1 and miR-140 in Regulating Growth  and Tumorigenesis via the TLR4/NF-kB Pathway in Cholangiocarcinoma},
JOURNAL = {Oncology Research},
VOLUME = {27},
YEAR = {2019},
NUMBER = {6},
PAGES = {663--672},
URL = {http://www.techscience.com/or/v27n6/48583},
ISSN = {1555-3906},
ABSTRACT = {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- B-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- B 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- B signaling axis in CCA tumorigenesis and progression but also denoted the 
probable utilization of SNHG1 as a therapeutic target for CCA.},
DOI = {10.3727/096504018X15420741307616}
}