101. Long noncoding RNA TP53TG1 suppresses the growth and metastasis of hepatocellular carcinoma by regulating the PRDX4/β-catenin pathway.
- Author
-
Chen, Baiyang, Lan, Jianwei, Xiao, Yusha, Liu, Pengpeng, Guo, Deliang, Gu, Yang, Song, Youai, Zhong, Qiu, Ma, Dong, Lei, Ping, and Liu, Quanyan
- Subjects
- *
LINCRNA , *HEPATOCELLULAR carcinoma , *INHIBITION of cellular proliferation , *METASTASIS , *EPITHELIAL-mesenchymal transition , *PROGNOSIS , *RNA metabolism , *RESEARCH , *LIVER tumors , *ANIMAL experimentation , *RESEARCH methodology , *CYTOSKELETAL proteins , *RETROSPECTIVE studies , *MEDICAL cooperation , *EVALUATION research , *COMPARATIVE studies , *OXIDOREDUCTASES , *CELL lines , *MICE - Abstract
Emerging evidence has shown that aberrant expression of lncRNA-TP53TG1 plays important roles in various malignancies. However, the biological functions of lncRNA-TP53TG1 in hepatocarcinogenesis, as well as the underlying mechanisms, remain largely unknown. Here, we assessed whether lncRNA-TP53TG1 plays a key role in the progression of hepatocellular carcinoma (HCC). The expression of lncRNA-TP53TG1 was significantly decreased in HCC tissues and cells. Decreased expression of lncRNA-TP53TG1 was associated with aggressive clinical phenotypes and a poor prognosis. Ectopic expression of lncRNA-TP53TG1 inhibited hepatoma cell proliferation and migration in vitro and in vivo, whereas lncRNA-TP53TG1 knockdown exerted the opposite effects. Furthermore, lncRNA-TP53TG1 played an important role in slowing the epithelial-mesenchymal transition (EMT) process in HCC. Mechanistically, lncRNA-TP53TG1 physically interacted with PRDX4 and promoted its ubiquitin-mediated degradation, resulting in the inactivation of the WNT/β-catenin signaling pathway in hepatoma cells. Our findings demonstrate a novel mechanism by which lncRNA-TP53TG1 exerts its tumor-suppressive effects through the WNT/β-catenin signaling pathway in a PRDX4-mediated manner in HCC. Based on these results, lncRNA-TP53TG1 potentially represents a prognostic indicator and therapeutic target for patients with HCC. [ABSTRACT FROM AUTHOR]
- Published
- 2021
- Full Text
- View/download PDF