MiR-744-5p inhibits the proliferation, invasion, and migration of clear-cell renal cell carcinoma cells by targeting CCND1.
10.12122/j.issn.1673-4254.2022.05.12
- Author:
Kun Yang LEI
1
;
Wen Jie XIE
1
;
Ting SUN
1
;
Yi Fu LIU
1
;
Xu WANG
2
Author Information
1. Department of Urology, First Affiliated Hospital of Nanchang University, Nanchang 330006, China.
2. Department of Pathology, First Affiliated Hospital of Nanchang University, Nanchang 330006, China.
- Publication Type:Journal Article
- Keywords:
CCND1;
clear-cell renal cell carcinoma;
miR-744-5p
- MeSH:
Carcinoma, Renal Cell/metabolism*;
Cell Line, Tumor;
Cell Movement/genetics*;
Cell Proliferation/genetics*;
Cyclin D1/genetics*;
Humans;
Kidney Neoplasms/metabolism*;
MicroRNAs/metabolism*
- From:
Journal of Southern Medical University
2022;42(5):712-717
- CountryChina
- Language:Chinese
-
Abstract:
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.
