Journal
ONCOTARGET
Volume 8, Issue 38, Pages 63724-63737Publisher
IMPACT JOURNALS LLC
DOI: 10.18632/oncotarget.18892
Keywords
HCC; LINC00052; EPB41L3; migration; invasion
Categories
Funding
- Major National ST Program [2013ZX10002002]
- major project of Chongqing Science & Technology Commission [cstc2013jcyjC10002]
- Natural Science Foundation Project of CQ CSTC [2010BB5359]
- Science and Technology Foundation of Guizhou province [[2016]1123]
- Science and Technology Cooperation Projects of Guizhou province [[2014]7005]
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Numerous studies have demonstrated that a class of long noncoding RNAs (lncRNAs) are dysregulated in hepatocellular carcinoma (HCC) and they are closely related with tumorigenesis. Our previous studies indicated that LINC00052 was a downregulated lncRNA in HCC and acted as a tumor suppressor gene. Using transcription microarray analysis, we found that knockdown of LINC00052 resulted in EPB41L3 downregulation. However, the function of EPB41L3 and the mechanism of LINC00052 downregulating EPB41L3 in HCC remain unclear. In this study, we found that overexpression of LINC00052 could upregulate the EPB41L3 expression and it might serve as a tumor suppressor gene in HCC. Database analysis showed that miR-452-5P could target LINC00052. The binding regions between LINC00052 and miR-452-5P were confirmed by luciferase assays. Moreover, LINC00052 inhibited cell malignant behavior by increasing miR-452-5P expression, suggesting that LINC00052 was negatively regulated by miR-452-5P. In addition, overexpression of miR-4525P resulted in a decrease of EPB41L3 expression, suggesting that EPB41L3 was as a target of miR-452-5P. In conclusion, these results demonstrated that a novel pathway was mediated by LINC00052 in HCC.
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