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LncRNA H19 inhibits proliferation and enhances apoptosis of nephroblastoma cells by regulating the miR-675/TGFBI axis.

Authors :
LIU, H.-C.
ZHU, W.-Y.
REN, L.-Y.
Source :
European Review for Medical & Pharmacological Sciences; 2022, Vol. 26 Issue 11, p3800-3806, 7p
Publication Year :
2022

Abstract

OBJECTIVE: To investigate the influences of long non-coding ribonucleic acid (lncRNA) H19 on proliferation and apoptosis of nephroblastoma cells. MATERIALS AND METHODS: A total of 5 pairs of nephroblastoma tissues and paraneoplastic tissues were obtained. Gene expression levels of lncRNA H19, microRNA (miR)-675, and transforming growth factor beta induced (TGFBI) were detected via quantitative Reverse Transcription-Polymerase Chain Reaction (qRT-PCR). Their regulatory effects on the viability of nephroblastoma cells were examined by Cell Counting Kit-8 (CCK-8) assay. Finally, the apoptosis level in each group was detected through TUNEL assay, and the protein expressions of TGFBI and Caspase-8 were examined using Western blotting (WB) assay. RESULTS: The gene expression levels of lncRNA H19 and miR-675 were markedly downregulated in nephroblastoma tissues (p<0.05), while that of TGFBI was notably upregulated (p<0.05). LncRNA H19 could reduce the proliferative ability of HFWT cells (p<0.05) and stimulates apoptosis rate (p<0.05). It upregulated the expressions of miR-675 and Caspase-8 (p<0.05), and downregulated TGFBI (p<0.05). Besides, miR-675 was able to upregulate Caspase-8 (p<0.05) and downregulate TGFBI (p<0.05). In addition, the protein expression of Caspase-8 was downregulated (p<0.05), while that of TGFBI was upregulated (p<0.05) after the knockdown of miR-675 in HFWT cells. CONCLUSIONS: LncRNA H19 may inhibit TGFBI expression by regulating miR-675 level, so as to weaken the proliferation and enhance the apoptosis of nephroblastoma cells. [ABSTRACT FROM AUTHOR]

Details

Language :
English
ISSN :
11283602
Volume :
26
Issue :
11
Database :
Supplemental Index
Journal :
European Review for Medical & Pharmacological Sciences
Publication Type :
Academic Journal
Accession number :
157469179