MiR-4443 promotes migration and invasion of breast cancer cells by inhibiting PEBP1 expression / 南方医科大学学报
Journal of Southern Medical University
;
(12): 1712-1719, 2020.
Artigo
em Chinês
| WPRIM
| ID: wpr-880802
ABSTRACT
OBJECTIVE@#To investigate the effect of miR-4443 expression on migration and invasion of breast cancer.@*METHODS@#We examined the expression of miR-4443 in breast carcinoma in situ and paired adjacent tissues from 3 breast cancer patients with high-throughput sequencing and verified the results using TCGA database. We also detected miR-4443 expressions using real-time quantitative PCR (RT-qPCR) in low invasive and highly invasive breast cancer cells (MCF-7 and MDA-MB-231 cells, respectively). The changes in apoptosis, migration and invasion of MCF-7 and MDA-MB-231 cells after transfection with miR-4443 mimics, mimics-NC, miR-4443 inhibitor or inhibitor-NC were analyzed using flow cytometry, wound healing assay and Transwell invasion assay. The target gene of miR-4443 was predicted by bioinformatics software and validated by a dual luciferase reporter gene system. RT-qPCR and Western blotting were performed to detect the expression of recombinant human phosphatidyl ethanolamine binding protein 1 (PEBP1) in the transfected cells.@*RESULTS@#The expression of miR-4443 was significantly higher in the breast cancer tissues than in the adjacent tissues (@*CONCLUSIONS@#MiR-4443 promotes the migration and invasion of breast cancer cells by inhibiting the expression of PEBP1, suggesting the possibility of suppressing miR-4443 expression as a potential therapeutic strategy for breast cancer.
Texto completo:
DisponíveL
Índice:
WPRIM (Pacífico Ocidental)
Assunto principal:
Neoplasias da Mama
/
Regulação Neoplásica da Expressão Gênica
/
Movimento Celular
/
MicroRNAs
/
Linhagem Celular Tumoral
/
Proteína de Ligação a Fosfatidiletanolamina
/
Proliferação de Células
/
Células MCF-7
/
Invasividade Neoplásica
Limite:
Humanos
Idioma:
Chinês
Revista:
Journal of Southern Medical University
Ano de publicação:
2020
Tipo de documento:
Artigo
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