MicroRNA‑584 directly targets CCND1 and inhibits cell proliferation and invasion in pancreatic cancer.
pancreatic cancer
microRNA-584
proliferation
invasion
cyclin D1
Journal
Molecular medicine reports
ISSN: 1791-3004
Titre abrégé: Mol Med Rep
Pays: Greece
ID NLM: 101475259
Informations de publication
Date de publication:
01 2019
01 2019
Historique:
received:
19
03
2018
accepted:
16
10
2018
pubmed:
16
11
2018
medline:
29
5
2019
entrez:
16
11
2018
Statut:
ppublish
Résumé
Multiple previous studies have demonstrated that the dysregulation of microRNAs (miRNAs) is implicated in the occurrence and development of pancreatic cancer. Therefore, a further characterisation of deregulated miRNAs in pancreatic cancer may provide novel insight into the oncogenesis and progression of pancreatic cancer, which may facilitate the identification of effective therapeutic targets for treating patients with this disease. In the present study, reverse transcription‑quantitative polymerase chain reaction analysis demonstrated that the expression level of miRNA‑584‑5p (miR‑584) was significantly decreased in pancreatic cancer tissues and cell lines. It was demonstrated that restoration of miR‑584 expression significantly suppressed the proliferative and invasive ability of pancreatic cancer cells. Bioinformatics analysis predicted that cyclin D1 (CCND1) was a putative target of miR‑584. Subsequent experiments demonstrated that CCND1 was a direct target gene of miR‑584 in pancreatic cancer cells. Furthermore, the inhibition of CCND1 mimicked the suppressive effect of miR‑584 overexpression in pancreatic cancer cells. The restoration of CCND1 expression significantly abolished the inhibitory effects of miR‑584 overexpression on pancreatic cancer cells. Collectively, the present results demonstrated that miR‑584 inhibited the development of pancreatic cancer by directly targeting CCND1, suggesting that this miRNA may represent a potential therapeutic target for this fatal disease.
Identifiants
pubmed: 30431107
doi: 10.3892/mmr.2018.9651
doi:
Substances chimiques
Biomarkers, Tumor
0
CCND1 protein, human
0
MIRN584 microRNA, human
0
MicroRNAs
0
Cyclin D1
136601-57-5
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM