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Non-Invasive PET/MR Imaging in an Orthotopic Mouse Model of Hepatocellular Carcinoma
Published on: August 31, 2022
lncRNA FEZF1‑AS1 contributes to cell proliferation, migration and invasion by sponging miR‑4443 in hepatocellular
Jianhua Gong1, Junyi Wang2, Tianpin Liu1
1Department of Hepatobiliary and Pancreatic Surgery, The First College of Clinical Medical Science, China Three Gorges University, Yichang, Hubei 443000, P.R. China.
Abstract:
As one of the most common and aggressive cancer types, hepatocellular carcinoma (HCC) leads to a large number of fatalities every year. However, the pathogenesis of HCC remains largely unknown. In the present study, it was identified that FEZF1‑AS1 was significantly upregulated in HCC cell lines and tissues, as determined by reverse transcription‑quantitative polymerase chain reaction. Additionally, it was observed that higher expression of FEZF1‑AS1 in patients with HCC indicated poorer prognosis. Furthermore, it was identified that knockdown of FEZF1‑AS1 markedly inhibited the proliferation, colony formation, migration and invasion of Hep3B and Huh7 cells, as determined by Cell Counting Kit‑8, colony formation and Transwell assays. In terms of mechanism, it was observed that FEZF1‑AS1 acted as a sponge for microRNA (miR)‑4443. The results of a luciferase reporter assay revealed that overexpression of miR‑4443 significantly inhibited the luciferase activity in Hep3B and Huh7 cells. Additionally, miR‑4443 overexpression markedly inhibited the expression of FEZF1‑AS1, and vice versa. It was additionally identified that miR‑4443 was downregulated in HCC tissues. There was an inverse correlation between the expression of miR‑4443 and FEZF1‑AS1 in HCC tissues. Furthermore, through functional experiments, it was identified that knockdown of FEZF1‑AS1 significantly inhibited the proliferation, migration and invasion of HCC cells, whereas inhibition of miR‑4443 reversed these effects. Collectively, the present results demonstrated that FEZF1‑AS1 acts as an oncogene by acting as a sponge for miR‑4443.
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