Long noncoding RNA MAFG‑AS1 promotes proliferation, migration and invasion of hepatocellular carcinoma cells through downregulation of miR‑6852
Long noncoding RNAs (lncRNAs) have been shown to participate in the development and progression of a number of different types of cancer, including hepatocellular carcinoma (HCC). A recent report has indicated that lncRNA MAFG-antisense 1 (AS1) promotes colorectal cancer. However, the role of MAFG-A...
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Published in | Experimental and therapeutic medicine Vol. 18; no. 4; pp. 2547 - 2553 |
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Main Authors | , , , |
Format | Journal Article |
Language | English |
Published |
Athens
Spandidos Publications
01.10.2019
Spandidos Publications UK Ltd D.A. Spandidos |
Subjects | |
Online Access | Get full text |
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Summary: | Long noncoding RNAs (lncRNAs) have been shown to participate in the development and progression of a number of different types of cancer, including hepatocellular carcinoma (HCC). A recent report has indicated that lncRNA MAFG-antisense 1 (AS1) promotes colorectal cancer. However, the role of MAFG-AS1 in other types of cancer remains unclear. The aim of the present study was to examine the effect of lncRNA MAFG-AS1 in HCC. Based on The Cancer Genome Atlas database and reverse transcription-quantitative PCR results, it was determined that lncRNA MAFG-AS1 expression was increased in HCC tissues and cell lines. Following knockdown of lncRNA MAFG-AS1, a Cell Counting Kit-8 assay and Transwell assay demonstrated that the proliferation, migration and invasion of HCC cell lines were significantly inhibited. It was additionally demonstrated that there was a negative regulatory association between lncRNA MAFG-AS1 and miR-6852. Inhibition of miR-6852 increased proliferation, migration and invasion of HCC cell lines. LncRNA MAFG-AS1 promoted HCC development by dampening miR-6852 function and may thus be a novel target for treating patients with HCC. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 1792-0981 1792-1015 |
DOI: | 10.3892/etm.2019.7850 |