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Circ_0000799 promotes proliferation and invasion in colorectal cancer and epithelial-mesenchymal transition

BACKGROUND: The current study aimed to investigate the effect of circ_0000799 on the biological function of colorectal cancer (CRC) cells and its mechanism. METHODS: First, quantitative reverse transcription polymerase chain reaction (qRT-PCR) was employed for detecting the expression of circ_000079...

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Detalles Bibliográficos
Autores principales: Geng, Chang-Hui, Zhang, Xue-Song, He, Miao, Gao, Ping, Zhao, Hong-Wei
Formato: Online Artículo Texto
Lenguaje:English
Publicado: AME Publishing Company 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9830346/
https://www.ncbi.nlm.nih.gov/pubmed/36636042
http://dx.doi.org/10.21037/jgo-22-1176
Descripción
Sumario:BACKGROUND: The current study aimed to investigate the effect of circ_0000799 on the biological function of colorectal cancer (CRC) cells and its mechanism. METHODS: First, quantitative reverse transcription polymerase chain reaction (qRT-PCR) was employed for detecting the expression of circ_0000799, miR-647, and miR-1243 in surgically resected specimens from hospitalized CRC patients, CRC-adjacent normal tissues (Normal group), human normal colon epithelial cells (FHC group), and CRC cell lines (HCT116, HT29, SW480, SW620). The cell proliferation, viability, and invasion were detected by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT), colony formation assay, transwell assay in HCT116 and SW480 cells with overexpression or inhibition of circ_0000799. The targeting relationship between circ_0000799 and miR-647 was verified by dual-luciferase reporter assay. The expression of epithelial-mesenchymal transition (EMT) proteins (E-cadherin, vimentin, and N-cadherin) was tested by western blot. RESULTS: The expression level of circ_0000799 was significantly increased in CRC tissues and cells. Overexpression of circ_0000799 significantly increased cell proliferation rate, viability, invasion, and the EMT process, whereas knockdown of circ_0000799 inhibited the biological performance of CRC cells. Bioinformatic analysis suggested that miR-647 was regulated by circ_0000799, and a dual-luciferase reporter assay further showed a targeting relationship between the two. In addition, circ_0000799 was negatively correlated with miR-647 expression in CRC. CONCLUSIONS: Our findings suggest that circ_0000799 promotes proliferation and invasion in CRC and EMT. These effects of circ_0000799 may be achieved by negatively regulating miR-62.