LncRNA H19 inhibits proliferation and enhances apoptosis of nephroblastoma cells by regulating the miR-675/TGFBI axis.
Eur Rev Med Pharmacol Sci
; 26(11): 3800-3806, 2022 06.
Article
en En
| MEDLINE
| ID: mdl-35731049
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.
Texto completo:
1
Colección:
01-internacional
Base de datos:
MEDLINE
Asunto principal:
Tumor de Wilms
/
MicroARNs
/
ARN Largo no Codificante
Límite:
Humans
Idioma:
En
Revista:
Eur Rev Med Pharmacol Sci
Asunto de la revista:
FARMACOLOGIA
/
TOXICOLOGIA
Año:
2022
Tipo del documento:
Article
País de afiliación:
China
Pais de publicación:
Italia