Background: Circ_0026344 was reported to be associated with the metastasis of colorectal cancer (CRC). This study aimed to investigate the expression of circ_0026344 in CRC and the effect mechanisms of circ_0026344 on CRC.Methods: The expressions of circ_0026344 and miR-31 in clinical CRC tissues or CRC cell lines were analyzed by qPCR. The target of circ_0026344 was predicted and verified by CircInteractome and dual-luciferase reporter assays. The correlation between circ_0026344 and miR-31 expression was analyzed using Pearson analysis. After the CRC cells were overexpressed circ_0026344 or miR-31 or silenced circ_0026344, the viability, apoptosis, migration, and invasion of CRC cells were evaluated by CCK-8, flow cytometry, wound healing, and transwell. Also, the expressions of miR-31, Bcl-2, Bax, E-cadherin, and N-cadherin in the cells were detected by qPCR or Western blot. Results: Circ_0026344 was low-expressed in CRC tissues and cell lines. Circ_0026344 sponged miR-31 which was high-expressed in CRC tissues. The expression of circ_0026344 was negatively correlated to the expression of miR-31. The miR-31 expression could be down-regulated by circ_0026344 overexpression. Circ_0026344 overexpression inhibited the cell viability, migration, and invasion; and enhanced the apoptosis of CRC cells. Circ_0026344 overexpression decreased the expressions of Bcl-2 and N-cadherin and increased the expressions of Bax and E-cadherin in CRC cells. Circ_0026344 silencing and miR-31 overexpression had an opposite effect on CRC cells as circ_0026344 overexpression. Furthermore, miR-31 overexpression counteracted the effect of circ_0026344 overexpression.Conclusion: Circ_0026344 overexpression inhibited the migration, invasion, and enhanced apoptosis of CRC cells by sponging miR-31.
Introduction:
Colorectal cancer (CRC) is hackneyed cancer and a major lethiferous cancer. Circular RNAs (CircRNAs) have been discovered to own important roles in controlling CRC progression. CircPSMC3 is known to exhibit lower expression in diversified cancers. However, the regulatory function of CircPSMC3 in CRC keeps unclear.
Methods:
The expression of CircPSMC3 and miR-31-5p was confirmed through RT-qPCR. The cell proliferation was measured through CCK-8 and EdU assays. The protein expression of genes was examined through a western blot. The cell invasion and migration were tested through Transwell and wound healing assays. The binding ability between CircPSMC3 and miR-31-5p was confirmed through the luciferase reporter assay.
objective:
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Results:
CircPSMC3 exhibited lower expression in CRC tissues and cell lines. Additionally, CircPSMC3 was revealed to suppress cell proliferation in CRC. Moreover, through Transwell and wound healing assays, CircPSMC3 was discovered to repress CRC cell invasion and migration. In CRC tissues, miR-31-5p expression was up-regulated and negatively correlated with CircPSMC3 expression. Further mechanism exploration experiments disclosed that CircPSMC3 is bound with miR-31-5p to modulate the YAP/β-catenin axis in CRC. At last, through rescue assays, CircPSMC3 inhibited cell proliferation, invasion and migration through sponging miR-31-5p in CRC.
Conclusion:
Our work was the first time to probe the potential regulatory effects of CircPSMC3 in CRC, and these above results uncovered that CircPSMC3 inhibited CRC cell growth and migration through regulating miR-31-5p/YAP/β-catenin. This discovery hinted that CircPSMC3 may serve as a useful therapeutic candidate for CRC.
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