[MiR-744-5p inhibits the proliferation, invasion, and migration of clear-cell renal cell carcinoma cells by targeting CCND1].
Nan Fang Yi Ke Da Xue Xue Bao
; 42(5): 712-717, 2022 May 20.
Article
en Zh
| MEDLINE
| ID: mdl-35673915
OBJECTIVE: To explore the role of miR-744-5p/CCND1 axis in clear-cell renal cell carcinoma (ccRCC). METHODS: We examined the expression levels of miR-744-5p in 65 pairs of ccRCC and adjacent tissue specimens and in 5 ccRCC cell lines and human renal tubular epithelial (HK2) cells using qRT-PCR. The ccRCC cell lines 786-O and OSRC2 were transfected with miR-744-5p mimic, CCND1 mimic, or their negative control mimics, and the changes in cell proliferation, migration, and invasion were evaluated with CCK-8, wound healing, and Transwell assays. The downstream target molecules of miR-744-5p were predicted by bioinformatics analysis, and the expression level of CCND1 in ccRCC cells was verified by qRT-PCR and Western blotting. The relationship between miR-744-5p and CCND1 was further validated by dual luciferase reporter assay, and the role of the miR-744-5p/CCND1 axis in ccRCC was explored by rescue experiments. RESULTS: MiR-744-5p was significantly downregulated in ccRCC tissues and cell lines (all P < 0.05), and its overexpression inhibited the proliferation, migration, and invasion of ccRCC cells (all P < 0.05). Bioinformatics analysis and dual luciferase reporter assay showed that CCND1 was a downstream target of miR-744-5p. The results of rescue experiments showed that upregulation of CCND1 could partially reverse the inhibitory effect of miR-744-5p overexpression on ccRCC cell proliferation, migration, and invasion (all P < 0.05). CONCLUSION: MiR-744-5p inhibits the malignant phenotype of ccRCC cells by targeting CCND1, and the miR-744-5p/CCND1 axis may be a novel target for diagnosis and treatment of ccRCC.
Palabras clave
Texto completo:
1
Base de datos:
MEDLINE
Asunto principal:
Carcinoma de Células Renales
/
MicroARNs
/
Neoplasias Renales
Límite:
Humans
Idioma:
Zh
Revista:
Nan Fang Yi Ke Da Xue Xue Bao
Año:
2022
Tipo del documento:
Article
País de afiliación:
China