Mechanism of long non-coding RNA MALAT1 in promoting migration of hepatocellular carcinoma cells
10.7644/j.issn.1674-9960.2017.06.001
- VernacularTitle:长链非编码RNA MALAT1促进肝癌细胞系迁移的机制研究
- Author:
Hui HAN
;
Haibei LI
;
Pengbo CAO
;
Geng QIN
;
Gangqiao ZHOU
- Keywords:
MALAT1;
liver neoplasms;
ceRNA;
neoplasm metastasis;
cell movement;
RNA;
small interfering;
genes;
neoplasm;
transfection
- From:
Military Medical Sciences
2017;41(6):409-414
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate whether the long non-coding RNA (lncRNA) metastasis associated lung adenocarcinoma transcript 1 (MALAT1) can act as a competitive endogenous RNA (ceRNA) to promote the migration of hepatocellular carcinoma (HCC) cells.Methods Transient transfection of small interfering RNA (siRNA) against MALAT1 was used to knockdown MALAT1 in HepG2 cells.Transwell assays were employed to assess the migration capabilities of HepG2 cells upon MALAT1 knockdown.RNA pull-down assays were performed to validate the direct binding between MALAT1 and miR-126*.Quantitative reverse transcription PCR (qRT-PCR) and Western blotting assays were used to detect the mRNA and protein levels of the miR-126* target genes.The dysregulation and prognostic significance of MALAT1 and miR-126* were analyzed in the public dataset of The Cancer Genome Atlas (TCGA).Results Compared with the control group, MALAT1 knockdown significantly inhibited the migration of HCC cells.MALAT1, with three miR-126* response elements, directly sponged miR-126* in a sequence-specific manner.The mRNA and protein levels of CXCL12, which was the miR-126* target gene, were significantly down-regulated upon MALAT1 knockdown.The TCGA database showed that MALAT1 was significantly up-regulated in HCC and high expression levels of MALAT1 were significantly associated with poor disease-free survival, whereas an opposite pattern of miR-126* was observed.Conclusion This study suggests that MALAT1 directly sponges miR-126* and upregulates the expression of CXCL12, which in turn promotes the migration of HCC cells.
