Hsa_circ_0079480 enhances cell proliferation, migration, and invasion in colorectal cancer through miR-498/ATP5E axis.
Kaohsiung J Med Sci
; 39(3): 209-220, 2023 Mar.
Article
em En
| MEDLINE
| ID: mdl-36625260
ABSTRACT
Circular RNAs play critical roles in tumorigenesis. hsa_circ_0079480 was reported to be upregulated in colorectal cancer (CRC). However, its specific molecule in CRC is poorly understood. Hsa_circ_0079480, miR-498, and ATP5E expressions in CRC tissues and CRC cells were determined using quantitative real-time polymerase chain reaction assay. ATP5E protein level was assessed using Western blot. Cell proliferation, migration, and invasion were examined by 3-(4, 5-Dimethylthiazolyl2)-2, 5-diphenyltetrazolium bromide assay and Transwell assays, respectively. Dual-luciferase reporter gene assay was performed to analyze the interactions between hsa_circ_0079480, miR-498, and ATP5E. This study results showed that hsa_circ_0079480 and ATP5E expressions were significantly increased in CRC tissues and CRC cells, while miR-498 was downregulated. Hsa_circ_0079480 knockdown dramatically suppressed CRC cell proliferation, migration, and invasion. Meanwhile, it turned out that hsa_circ_0079480 knockdown inhibited CRC tumor growth in vivo. Hsa_circ_0079480 could negatively regulate miR-498 expression by directly targeting miR-498. MiR-498 overexpression dramatically inhibited CRC cell malignant behaviors. miR-498 negatively regulated ATP5E expression by directly binding to ATP5E. ATP5E knockdown suppressed CRC cell malignant behaviors. ATP5E overexpression mitigated the inhibitory effect of hsa_circ_0079480 on CRC cell malignant behaviors. Since hsa_circ_0079480 knockdown inhibited CRC cells malignant behaviors through regulation of the miR-498/ATP5E axis, it can be concluded that hsa_circ_0079480 might have great potential as therapeutic target for CRC.
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Texto completo:
1
Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Neoplasias Colorretais
/
MicroRNAs
Limite:
Humans
Idioma:
En
Ano de publicação:
2023
Tipo de documento:
Article