OBJECTIVE: Hepatocellular carcinoma (HCC) is an invasive malignant tumor with high mortality rate. Long non-coding RNA (lncRNA) MAFG-AS1 has been showed to play an oncogenic role in several malignant tumors. Nonetheless, the exact role of MAFG-AS1 in the progression of HCC has not been fully elucidated. PATIENTS AND METHODS: Real-time quantitative polymerase chain reaction (RT-qPCR) and Western blot were used to detect the mRNA and protein expression of MAFG-AS1 in HCC tissues and cells. Cell counting kit-8 (CCK-8), transwell and tubule formation assays were applied to uncover the proliferation, migration, invasion and tumor angiogenesis of HCC cells, respectively. RNA binding protein immunoprecipitation (RIP) assay and Luciferase reporter gene assay were employed to explore the molecular mechanism. In addition, Xenograft assay was used to investigate the effect of MAFG-AS1 in vivo. RESULTS: MAFG-AS1 was highly expressed in HCC tissues and cells. Attenuation of MAFG-AS1 evidently suppressed the proliferation, migration, invasion and tumor angiogenesis of HCC cells, suggesting that MAFG-AS1 played an oncogenic role in HCC. MiR-3196 was sponged by MAFG-AS1, and OTX1 was a downstream target of miR-3196 in HCC. In addition, OTX1 expression was negatively associated with miR-3196 but positively associated with MAFG-AS1 in HCC tissues. Overexpression of OTX1 could abolish the repressive influence of MAFG-AS1 inhibition on the proliferation, migration, invasion and tumor angiogenesis of HCC cells. CONCLUSIONS: MAFG-AS1 facilitated the progression of HCC via targeting miR-3196/OTX1 axis, which might be used as a new insight for HCC treatment.
OBJECTIVE:Hepatocellular carcinoma (HCC) is an invasive malignant tumor with high mortality rate. Long non-coding RNA (lncRNA) MAFG-AS1 has been showed to play an oncogenic role in several malignant tumors. Nonetheless, the exact role of MAFG-AS1 in the progression of HCC has not been fully elucidated. PATIENTS AND METHODS: Real-time quantitative polymerase chain reaction (RT-qPCR) and Western blot were used to detect the mRNA and protein expression of MAFG-AS1 in HCC tissues and cells. Cell counting kit-8 (CCK-8), transwell and tubule formation assays were applied to uncover the proliferation, migration, invasion and tumor angiogenesis of HCC cells, respectively. RNA binding protein immunoprecipitation (RIP) assay and Luciferase reporter gene assay were employed to explore the molecular mechanism. In addition, Xenograft assay was used to investigate the effect of MAFG-AS1 in vivo. RESULTS:MAFG-AS1 was highly expressed in HCC tissues and cells. Attenuation of MAFG-AS1 evidently suppressed the proliferation, migration, invasion and tumor angiogenesis of HCC cells, suggesting that MAFG-AS1 played an oncogenic role in HCC. MiR-3196 was sponged by MAFG-AS1, and OTX1 was a downstream target of miR-3196 in HCC. In addition, OTX1 expression was negatively associated with miR-3196 but positively associated with MAFG-AS1 in HCC tissues. Overexpression of OTX1 could abolish the repressive influence of MAFG-AS1 inhibition on the proliferation, migration, invasion and tumor angiogenesis of HCC cells. CONCLUSIONS:MAFG-AS1 facilitated the progression of HCC via targeting miR-3196/OTX1 axis, which might be used as a new insight for HCC treatment.