miR-130b suppresses the invasion and migration of prostate cancer via inhibiting DLL1 and regulating the PI3K/Akt pathways.
Exp Ther Med
; 23(1): 98, 2022 Jan.
Article
em En
| PubMed-not-MEDLINE
| ID: mdl-34976140
Prostate cancer occurs in the prostatic epithelium and poses a threat to the health of middle-aged and older males. The objective of the present study was to explore the roles of microRNA (miRNA/miR)-130b in prostate cancer and potential molecular mechanisms in order to control the migration and invasion of prostate cancer. For this purpose, reverse transcription-PCR was performed to evaluate the mRNA levels of DLL1, phosphoinositide-3 kinase (PI3K), protein kinase B (Akt) and matrix metalloproteinase (MMP)9, and western blot analysis was carried out to detect the protein expression levels of DLL1, phosphorylated (p)-PI3K, p-Akt and MMP9. A Transwell assay was conducted to examine the invasion rate of prostate cancer cells. Furthermore, a scratch wound assay was performed to examine the migration rate of prostate cancer cells. A luciferase assay was performed to examine the interaction between miRNA and its target mRNA. The results revealed that miR-130b had abnormal (low) expression in tumor tissues compared with that in the adjacent normal tissue. An miR-130b mimic suppressed the expression of DLL1. The expression of p-PI3K, p-Akt and MMP9 in prostate cancer cells transfected with the miR-130b mimic was decreased in comparison to the negative control and control groups. Furthermore, migration and invasion were significantly suppressed in the miR-130b mimic group. In conclusion, a novel pathway interlinking miR-130b and MMP9, p-Akt and p-PI3K, which regulates the migration and invasion of prostate cancer cells, was identified. These ï¬ndings provide an intriguing biomarker and treatment strategy for patients with prostate cancer.
Texto completo:
1
Coleções:
01-internacional
Temas:
Geral
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Tipos_de_cancer
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Prostata
Base de dados:
MEDLINE
Idioma:
En
Revista:
Exp ther med
Ano de publicação:
2022
Tipo de documento:
Article