KMID : 0381120190410080951
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Genes and Genomics 2019 Volume.41 No. 8 p.951 ~ p.959
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Down-regulation expression of TGFB2-AS1 inhibits the proliferation, migration, invasion and induces apoptosis in HepG2 cells
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Liu Wenrong
Huai Ruiping Zhang Yin Rao Shuquan Xiong Lili Ding Ruofan Mao Canquan Zhao Wenqing Hao Tao Huang Qingqing Guo Zhiyun
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Abstract
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Background: Hepatocellular carcinoma (HCC) is the leading cause of cancer mortality and without effective prognosis. Previous study has been confirmed that the abnormal expression of long non-coding RNAs (lncRNAs) TGFB2-AS1 was involved in tumorigenesis. However, the biological functions of TGFB2-AS1 in hepatocellular carcinoma (HCC) remain largely unclear.
Objective: We comprehensively assess the clinical significance of TGFB2-AS1 and investigate the biological functions of TGFB2-AS1 on HCC HepG2 cells.
Methods: We firstly confirmed the expression of TGFB2-AS1 between tumor and normal tissues using public available transcriptome data. We analyzed the clinical significance of TGFB2-AS1 using the TCGA HCC datasets. The biological functions of TGFB2-AS1 on HCC HepG2 cells were explored by multiple in vitro assays.
Results: We found that TGFB2-AS1 was remarkably increased in HCC tissues (P?=?0.00148) and exhibited a potential predictive marker for HCC, with an area under curve (AUC) of 0.708 (P?=?0.0034) using the fifty pairs of matched HCC tissues of TCGA. Besides, higher expression of TGFB2-AS1 in HCC tissues was identified as being positively associated with advanced tumor (P?=?0.012) and disease stage (P?=?0.009) in 355 HCC cases using independent sample nonparametric test. Downregulation of TGFB2-AS1 expression significantly restrained proliferation (P?0.01) and impaired colony formation (P?0.05). Furthermore, TGFB2-AS1 depletion remarkably promoted the apoptosis of HepG2 cells (P?0.05) and inhibited migration and invasion (P?0.01).
Conclusion: Taken together, these findings suggested that TGFB2-AS1 might serve as a potential therapeutic target for HCC.
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KEYWORD
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Long non-coding RNA, Hepatocellular carcinoma, Bioinformatics, Proliferation, Apoptosis, Migration
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