MiR-98-5p regulates proliferation and metastasis of MCF-7 breast cancer cells by targeting Gab2.
Eur Rev Med Pharmacol Sci
; 23(7): 2847-2855, 2019 Apr.
Article
en En
| MEDLINE
| ID: mdl-31002135
ABSTRACT
OBJECTIVE:
The aim of this study was to explore the mechanism of miR-98-5p in influencing the malignant proliferation and metastasis capacities of breast cancer cells. PATIENTS ANDMETHODS:
Quantitative Reverse Transcription-Polymerase Chain Reaction (qRT-PCR) was used to detect the expression level of miR-98-5p and GRB2-associated-binding protein 2 (Gab2) in breast cancer samples and cells. On-line target gene prediction software and Dual-Luciferase reporter assay were used to predict and verify the target genes of miR-98-5p, respectively. Cell proliferation was measured by MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide) assay. Meanwhile, migration and invasion abilities, as well as the changes of epithelial-mesenchymal transition (EMT) after transfection were detected by transwell assay and Western blot assay, respectively.RESULTS:
Compared with adjacent non-tumor tissues and MCF-10A cells, the expression level of miR-98-5p in tumor tissues and MCF-7 cells was significantly declined, whereas Gab2 was markedly up-regulated. Besides, Gab2 was predicted as a target gene of miR-98-5p. Subsequent experiments indicated that the proliferation, migration, invasion and EMT of MCF-7 cells transfected with miR-98-5p were significantly inhibited. However, up-regulation of Gab2 attenuated the biological function of miR-98-5p on malignant abilities of breast cancer cells.CONCLUSIONS:
We showed that miR-98-5p served as anti-oncogene in breast cancer, which might provide a new therapeutic target for its treatment.
Texto completo:
1
Colección:
01-internacional
Base de datos:
MEDLINE
Asunto principal:
Neoplasias de la Mama
/
MicroARNs
/
Células MCF-7
Tipo de estudio:
Prognostic_studies
Límite:
Female
/
Humans
Idioma:
En
Revista:
Eur Rev Med Pharmacol Sci
Asunto de la revista:
FARMACOLOGIA
/
TOXICOLOGIA
Año:
2019
Tipo del documento:
Article
País de afiliación:
China