@Article{096504017X14920318811749,
AUTHOR = {Li Lv, Jian-Qin Jia, Jin Chen},
TITLE = {The lncRNA CCAT1 Upregulates Proliferation and Invasion  in Melanoma Cells via Suppressing miR-33a},
JOURNAL = {Oncology Research},
VOLUME = {26},
YEAR = {2018},
NUMBER = {2},
PAGES = {201--208},
URL = {http://www.techscience.com/or/v26n2/56631},
ISSN = {1555-3906},
ABSTRACT = {It is increasingly evident that various long noncoding RNAs (lncRNAs) participate in the tumorigenesis of 
multiple tumors, including melanoma. lncRNAs have been validated as oncogenic factors in various tumors; 
however, the potential regulatory mechanism of CCAT1 in melanoma is still unclear. The purpose of this 
study was to investigate the regulation of CCAT1 on melanoma genesis. The expression of CCAT1 in melanoma tissue and cell lines was measured using qRT-PCR. Interference oligonucleotide or mimic sequences 
were applied to up- or downregulate RNA expression. CCK-8 and colony formation assays were performed to 
detect the proliferation capability. Transwell assay was used to assess the migration and invasion capacities. 
Bioinformatics analysis was performed to predict the target miRNAs of CCAT1. Expression of CCAT1 was 
significantly upregulated in melanoma tissue and cell lines. CCAT1 knockdown observably suppressed the 
proliferation, migration, and invasion abilities. Bioinformatics analysis predicted that miR-33a acted as a target 
of CCAT1, which was confirmed by dual-luciferase reporter assay. CCAT1 knockdown reversed the tumorpromoting ability of the miR-33a inhibitor. CCAT1 acts as an oncogenic factor in the genesis of melanoma and 
exerts tumor-promoting roles via sponging miR-33a, providing a novel insight for competing endogenous RNA 
(ceRNA) in the tumorigenesis of melanoma.},
DOI = {10.3727/096504017X14920318811749}
}