Background
Colorectal cancer (CRC) is a common malignant tumor in digestive system. Circular RNA (circRNA) circ_0007142 has been identified as an oncogene in CRC. However, the mechanism of circ_0007142 in CRC was rarely reported. Materials and
Conclusion
Circ_0007142 modulated CDC25A expression to promote CRC progression by sponging miR-122-5p.
Methods
The levels of circ_0007142, dedicator of cytokinesis 1 (DOCK1), microRNA-122-5p (miR-122-5p), and cell division cycle 25A (CDC25A) in CRC tissues (n=31) and cells were examined by quantitative real-time polymerase chain reaction (qRT-PCR). The cell viability and colony-forming ability were evaluated via 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide (MTT) assay and colony-formation assay, respectively. The migrated and invaded abilities were monitored by Transwell assay. The dual-luciferase reporter assay was performed to validate the interactions between miR-122-5p and circ_0007142 or CDC25A. The protein level of CDC25A was detected via Western blot assay. The biological role of circ_0007142 was examined by xenograft tumor model in vivo.
Results
The levels of circ_0007142 and CDC25A were enhanced and the level of miR-122-5p was declined in CRC tissues and cells, while the level of DOCK1 had no fluctuation. Circ_0007142 sponged miR-122-5p and CDC25A was a target of miR-122-5p. Circ_0007142 knockdown impeded cell proliferation, colony formation, migration, and invasion in CRC cells by regulating miR-122-5p. Besides, miR-122-5p inhibitor promoted cell proliferation, colony formation, migration, and invasion in CRC cells by modulating CDC25A. Circ_0007142 regulated CDC25A expression in CRC cells by sponging miR-122-5p. Moreover, circ_0007142 knockdown blocked CRC tumor growth in vivo.