Abstract
Introduction Colorectal cancer (CRC), a common digestive tract tumor that contains colon and rectal cancer, is one of the three most common cancers globally. circRNAs are involved in the occurrence and development of CRC, but the mechanism of how they participate in this process remains unclear. Methods We adopted PCR for expression measure, CCK-8 for cell proliferation detection, Transwell for cell migration and invasion detection, and dual-luciferase reporter assays to detect the potential downstream targets of CCDC66 in CRC. Results This study showed that circRNA CCDC66 was overexpressed in CRC tissues, and after knockdown, it inhibited the proliferation, migration, and invasion of CRC cells (RKO and HCT-116) in vitro. In addition, the dual-luciferase reporter assay showed that there was a binding site between circCCDC66 and miR-370, as well as between miR-370 and murine double minute 4 (MDM4). That is, circCCDC66 upregulated the expression of MDM4 through competitively binding to miR-370. The expression of circCCDC66 in CRC tissues was positively correlated with MDM4 and negatively correlated with miR-370. Conclusion In summary, our results indicate that circCCDC66 is a key upregulation of CRC. circCCDC66 upregulates MDM4 through competitive binding to miR-370, thereby enhancing the metastatic ability of CRC cells and promoting the development of CRC.
Highlights
Colorectal cancer (CRC), a common digestive tract tumor that contains colon and rectal cancer, is one of the three most common cancers globally. circRNAs are involved in the occurrence and development of CRC, but the mechanism of how they participate in this process remains unclear
The circRNAs play a crucial role in CRC development and progression. circITGA7 sponges miR3187-3p via its miR-3187-3p targeting sites to regulate CRC progression [11]. circRNA_100290 is capable of binding to miR-516b directly and promoting migration, invasion, and proliferation of CRC cells in vitro through decreasing the expression of FZD4 [12]. circFOXO3 acts as a miR-29a-3p sponge to exhibit oncogenic activity that affects the cell cycle and cell apoptosis in prostate cancer through transcriptional upregulation of SLC25A15 [13]
We found that the expression of circCCDC66 in CRC tissues increased
Summary
Colorectal cancer (CRC), a common digestive tract tumor that contains colon and rectal cancer, is one of the three most common cancers globally. circRNAs are involved in the occurrence and development of CRC, but the mechanism of how they participate in this process remains unclear. This study showed that circRNA CCDC66 was overexpressed in CRC tissues, and after knockdown, it inhibited the proliferation, migration, and invasion of CRC cells (RKO and HCT-116) in vitro. The dual-luciferase reporter assay showed that there was a binding site between circCCDC66 and miR370, as well as between miR-370 and murine double minute 4 (MDM4). CircCCDC66 upregulated the expression of MDM4 through competitively binding to miR-370. CircCCDC66 upregulates MDM4 through competitive binding to miR-370, thereby enhancing the metastatic ability of CRC cells and promoting the development of CRC. CircRNA_100290 is capable of binding to miR-516b directly and promoting migration, invasion, and proliferation of CRC cells in vitro through decreasing the expression of FZD4 [12]. We would like to resolve the secret role of circCCDC66 in CRC and further elucidate the mechanism at a molecular level
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