@Article{096504021X16310057751016,
AUTHOR = {Ziyi Wang, Xinyu Zhang, Xuedong Zhang, Xuedong Jiang, Wenya Li},
TITLE = {Long Noncoding RNA LINC01703 Exacerbates the Malignant Properties  of Non-Small Cell Lung Cancer by Upregulating MACC1  in a MicroRNA-605-3p-Mediated Manner},
JOURNAL = {Oncology Research},
VOLUME = {28},
YEAR = {2020},
NUMBER = {9},
PAGES = {913--927},
URL = {http://www.techscience.com/or/v28n9/48485},
ISSN = {1555-3906},
ABSTRACT = {Long intergenic nonprotein-coding RNA 1703 (LINC01703) has diagnostic significance in lung adenocarcinoma. However, its specific roles in non-small cell lung cancer (NSCLC) and downstream mechanisms have 
not been investigated. In the current study, we characterized the role of LINC01703 in NSCLC malignancy 
and elucidated its detailed mechanism of action. LINC01703 expression was measured by qRT-PCR. The 
regulatory effects of LINC01703 on the malignancy of NSCLC cells were assessed by multiple functional 
experiments. The targeted interaction was confirmed by RNA immunoprecipitation and luciferase reporter 
assays. Herein, overexpression of LINC01703 in NSCLC was indicated in the TCGA database and further 
proven in our cohort. Functional studies revealed that knocking down LINC01703 repressed cell proliferation, 
colony formation, migration, and invasion in vitro, which was accompanied by the induction of apoptosis. 
The tumor growth of LINC01703-silenced cells was also inhibited in vivo. Mechanistic analyses revealed that 
LINC01703 functioned as a competing endogenous RNA for microRNA-605-3p (miR-605-3p) in NSCLC 
cells, which thereby upregulated the miR-605-3p target metastasis associated with colon cancer 1 (MACC1). 
Rescue experiments highlighted that the regulatory actions of LINC01703 ablation on NSCLC cells were 
abolished in response to miR-605-3p downregulation or MACC1 overexpression. In conclusion, LINC01703 
enhanced the aggressiveness of NSCLC cells by altering miR-605-3p/MACC1. Our work suggests the therapeutic potential of LINC01703/miR-605-3p/MACC1 in NSCLC.},
DOI = {10.3727/096504021X16310057751016}
}