@Article{096504017X14953948675403,
AUTHOR = {Shujun Liu, Guigang Yan, Junfu Zhang, Lianzhi Yu},
TITLE = {Knockdown of Long Noncoding RNA (lncRNA) Metastasis-Associated  Lung Adenocarcinoma Transcript 1 (MALAT1) Inhibits Proliferation,  Migration, and Invasion and Promotes Apoptosis by Targeting  miR-124 in Retinoblastoma},
JOURNAL = {Oncology Research},
VOLUME = {26},
YEAR = {2018},
NUMBER = {4},
PAGES = {581--591},
URL = {http://www.techscience.com/or/v26n4/56671},
ISSN = {1555-3906},
ABSTRACT = {Evidence suggests that the long noncoding RNA (lncRNA) metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) is upregulated in cancer tissues, and its elevated expression is associated with hyperproliferation. However, the underlying mechanisms regarding the role of MALAT1 in retinoblastoma (RB) remain 
unclear. This study aimed to explore the functional role of MALAT1 in RB by targeting miR-124. The results 
showed that the expression of MALAT1 was significantly higher in the Y79 cell line than in the ARPE-19 cell 
line (<i>p</i><0.01). Moreover, MALAT1 silence inhibited cell viability, migration, and invasion and promoted apoptosis in Y79 cells (<i>p</i>< 0.05, <i>p</i><0.01, or <i>p</i><0.001). miR-124 was upregulated by MALAT1 silence and hence 
was identified as a target of MALAT1 (<i>p</i><0.05 or <i>p</i><0.001). In addition, miR-124 suppression inhibited cell 
apoptosis and remarkably abolished the inhibitory effects of MALAT1 silence on cell viability, migration, 
and invasion (<i>p</i>< 0.05, <i>p</i><0.01, or <i>p</i><0.001). In addition, Slug was a target of miR-124 and regulated cell 
viability, migration, invasion, and apoptosis in Y79 cells (<i>p</i>< 0.05, <i>p</i><0.01, or <i>p</i><0.001). Further, Slug silence 
abolished miR-124 suppression-induced inactivation of the ERK/MAPK and Wnt/β-catenin pathways. Taken 
together, our data highlight the pivotal role of MALAT1 in RB. Moreover, the present study elucidated the 
MALAT1–miR-124–ERK/MAPK and Wnt/β-catenin signaling pathways in RB, which might provide a new 
approach for the treatment of RB.},
DOI = {10.3727/096504017X14953948675403}
}