C Shen1, Y Xu, T-F Lu, J-J Zhang, Y-B Qian, N Xu. 1. Department of Liver Surgery, Renji Hospital Affiliated to Shanghai Jiaotong University School of Medicine, Shanghai, China. xuning@renji.com.
Abstract
OBJECTIVE: To clarify the potential effect of long non-coding RNA (lncRNA) TATDN1 on accelerating the proliferative rate and cell cycle progression of hepatocellular carcinoma (HCC) via sponging miRNA-6089, thus participating in the progression of HCC. PATIENTS AND METHODS: TATDN1 expression in HCC tissues and normal tissues was first determined by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). The correlation between TATDN1 expression to metastasis and overall survival of HCC was analyzed. The cellular level of TATDN1 in HCC cell lines was examined as well. Regulatory effects of TATDN1 on cell cycle progression and viability of HepG2 and SMMC7721 cells were evaluated. Subsequently, a potential target of TATDN1 was screened out and verified by Dual-Luciferase reporter gene assay. The expression pattern and biological function of the target gene miRNA-6089 in HCC were also determined. In a similar way, LIX1L was verified to be the target of miRNA-6089 and tested for its biological function in HCC. RESULTS: TATDN1 was upregulated in HCC tissues and cell lines. The overexpression of TATDN1 accelerated the proliferative rate and cell cycle progression of HCC. MiRNA-6089, the target gene of TATDN1, was lowly expressed in HCC. The overexpression of miRNA-6089 partially reversed the promotive role of TATDN1 in regulating the proliferation and cell cycle of HCC cells. Subsequently, LIX1L was verified to be the target of miRNA-6089. The overexpression of LIX1L partially reversed the regulatory effect of miRNA-6089 on the proliferative rate and cell cycle progression of HCC. CONCLUSIONS: TATDN1 accelerates the proliferative rate and cell cycle progression of HCC by degrading miRNA-6089 to upregulate LIX1L.
OBJECTIVE: To clarify the potential effect of long non-coding RNA (lncRNA) TATDN1 on accelerating the proliferative rate and cell cycle progression of hepatocellular carcinoma (HCC) via sponging miRNA-6089, thus participating in the progression of HCC. PATIENTS AND METHODS: TATDN1 expression in HCC tissues and normal tissues was first determined by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). The correlation between TATDN1 expression to metastasis and overall survival of HCC was analyzed. The cellular level of TATDN1 in HCC cell lines was examined as well. Regulatory effects of TATDN1 on cell cycle progression and viability of HepG2 and SMMC7721 cells were evaluated. Subsequently, a potential target of TATDN1 was screened out and verified by Dual-Luciferase reporter gene assay. The expression pattern and biological function of the target gene miRNA-6089 in HCC were also determined. In a similar way, LIX1L was verified to be the target of miRNA-6089 and tested for its biological function in HCC. RESULTS:TATDN1 was upregulated in HCC tissues and cell lines. The overexpression of TATDN1 accelerated the proliferative rate and cell cycle progression of HCC. MiRNA-6089, the target gene of TATDN1, was lowly expressed in HCC. The overexpression of miRNA-6089 partially reversed the promotive role of TATDN1 in regulating the proliferation and cell cycle of HCC cells. Subsequently, LIX1L was verified to be the target of miRNA-6089. The overexpression of LIX1L partially reversed the regulatory effect of miRNA-6089 on the proliferative rate and cell cycle progression of HCC. CONCLUSIONS:TATDN1 accelerates the proliferative rate and cell cycle progression of HCC by degrading miRNA-6089 to upregulate LIX1L.