Down-regulation expression of TGFB2-AS1 inhibits the proliferation, migration, invasion and induces apoptosis in HepG2 cells.

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.