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lncRNA TMPO-AS1 Exerts Oncogenic Roles in HCC Through Regulating miR-320a/SERBP1 Axis.
- Source :
-
OncoTargets & Therapy . Jul2020, Vol. 13, p6539-6551. 13p. - Publication Year :
- 2020
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Abstract
- Background: Previous evidence have shown that long non-coding RNA (lncRNA) TMPO antisense RNA 1 (TMPO-AS1) is involved in the aggressiveness of several cancers. Nevertheless, the precise functions of TMOP-AS1 in hepatocellular carcinoma (HCC) are still unresolved. Materials and Methods: The expressions of TMPO-AS1 and miR-320a were detected in HCC tissues and cells by qRT-RCR. The cell growth, migration and invasion were detected by colony formation, wound healing assay and Transwell assay, respectively. The targeting relation between miR-320a and TMPO-AS1 was predicted by bioinformatics analysis and identified by luciferase reporter gene as well as FISH assay. The expression of SERPINE1 MRNA Binding Protein 1 (SERBP1) was detected by Western blot. The growth of HCC cell was analyzed using transplanted tumor model. Results: Currently, we revealed that TMPO-AS1 was overexpressed in clinical HCC samples and a panel of HCC cell lines. Clinically, a higher level of TMPO-AS1 was connected to the advanced stage of HCC and worse prognosis of patients. Depletion of TMPO-AS1 repressed HCC cell viability, migration ability and invasiveness. Nevertheless, upregulation of TMPO-AS1 caused opposite results. Further studies revealed that lncRNA TMPO-AS1 was largely located in the cytoplasm of HCC cell and sponge miR-320a, resulting in increasing the level of SERBP1 in HCC cell. Finally, TMPO-AS1 silencing suppressed tumor growth of HCC cell in vivo. Conclusion: Collectively, our results suggested that TMPO-AS1 was a promoting factor for the aggressive behaviors of HCC cell. [ABSTRACT FROM AUTHOR]
Details
- Language :
- English
- ISSN :
- 11786930
- Volume :
- 13
- Database :
- Academic Search Index
- Journal :
- OncoTargets & Therapy
- Publication Type :
- Academic Journal
- Accession number :
- 145263919
- Full Text :
- https://doi.org/10.2147/OTT.S250355