Role of lncRNA NR2F1-AS1 and lncRNA H19 Genes in Hepatocellular Carcinoma and Their Effects on Biological Function of Huh-7
This research was designed to probe into the expression and related mechanism of lncRNA NR2F1-AS1 and H19 in hepatocellular carcinoma (HCC). Forty-two HCC patients who came to our hospital from February 2018 to August 2019 were included into a research group (RG). Meanwhile, 46 healthy controls were...
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Veröffentlicht in: | Cancer management and research 2021-01, Vol.13, p.941-951 |
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Zusammenfassung: | This research was designed to probe into the expression and related mechanism of lncRNA NR2F1-AS1 and H19 in hepatocellular carcinoma (HCC).
Forty-two HCC patients who came to our hospital from February 2018 to August 2019 were included into a research group (RG). Meanwhile, 46 healthy controls were regarded as a control group (CG). BEL-7402, Huh-7 human hepatoma cells and HL-7702 human normal liver cells were purchased, and the NR2F1-AS1 and H19 levels in serum and tissues of HCC patients were detected. PcDNA3.1-NR2F1-AS1, si-NR2F1-AS1, NC, pcDNA3.1-H19 and si-H19 were transfected into BEL-7402 and Huh-7 cells. The NR2F1-AS1 and H19 levels in samples were detected via qRT-PCR, and the expression of apoptosis-related proteins in cells was tested through WB. Cell proliferation, invasion, or apoptosis was detected by CCK8, Transwell or flow cytometry, respectively.
The NR2F1-AS1 and H19 levels were high in human hepatoma cells, and AUCs of lncRNA NR2F1-AS1 and lncRNA H19 were both >0.8. The lncRNA NR2F1-AS1 and lncRNA H19 were associated with HCC staging. After transfection of pcDNA3.1-NR2F1-AS1, si-NR2F1-AS1, NC, pcDNA3.1-H19, si-H19 BEL-7402 and Huh-7 cells, silencing NR2F1-AS1 and H19 expression can promote apoptosis and inhibit cell growth, while silencing their over-expression can inhibit the EMT process of Huh-7 cells.
lncRNA NR2F1-AS1 and lncRNA H19 genes are abnormally expressed in HCC. Furthermore, the two can suppress the EMT process of Huh-7 cells and promote apoptosis effectively. |
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ISSN: | 1179-1322 1179-1322 |
DOI: | 10.2147/CMAR.S284650 |