Published online Sep 28, 2021. doi: 10.3748/wjg.v27.i36.6064
Peer-review started: March 3, 2021
First decision: June 3, 2021
Revised: June 4, 2021
Accepted: August 9, 2021
Article in press: August 9, 2021
Published online: September 28, 2021
Processing time: 203 Days and 23.4 Hours
Colorectal cancer (CRC) is the third most common cancer and the second most common cause of cancer-related death worldwide. Recent studies have shown that circular RNAs play important roles in regulating the progression of CRC. However, the biological role and underlying mechanism of circRNA_0084927 (circ_0084927) in CRC remain unclear.
Due to tumor metastasis and other complications, the 5-year survival rate of patients with advanced-stage CRC is very low. We hope to provide a new treatment strategy for CRC with metastasis.
The present study aimed to investigate the role and mechanism of circ_0084927 in regulating the progression of CRC.
Clinical tissue samples and cells were collected, and the expression of circ_0084927 was detected by quantitative polymerase chain reaction (qPCR) The diagnostic performance of circ_0084927 was assessed by receiver operating characteristic curve analysis. The role of circ_0084927 in proliferation, migration, and invasion was determined using cell counting kit-8 assay, wound healing assay, and transwell assay, respectively. The regulatory relationship among circ_0084927, miRNA-20b-3p (miR-20b-3p), and glutathione S-transferase mu 5 (GSTM5) was identified using databases, luciferase reporter assays, qPCR, and Western blot analysis. AKT-mTOR signaling was also verified after circ_0084927 knockdown or miR-20b-3p mimic treatment.
The expression of circ_0084927 was significantly increased in CRC tissues and cells, and was increased in advanced-stage CRC compared with in early-stage CRC. The area under the curve (AUC) of circ_0084927 was 0.806 (95%CI: 0.683 to 0.896). In addition, the AUC was 0.874 (95%CI: 0.738-0.956) in patients with advanced-stage CRC and 0.713 (95%CI: 0.555-0.840) in those with early-stage CRC. Knockdown of circ_0084927 inhibited the migration and invasion of HCT116 cells. Moreover, circ_0084927 was found to act as a sponge of miR-20b-3p. MiR-20b-3p activation reduced the circ_0084927 level, whereas miR-20b-3p inhibition increased the circ_0084927 level. But the effect was not found after circ_0084927 mutation. In addition, miR-20b-3p expression in CRC patients was also reduced and negatively correlated with circ_0084927 expression. The function of circ_0084927 in HCT116 cells with circ_0084927 knockdown was rescued by miR-20b-3p. Moreover, GSTM5 expression was significantly decreased after overexpressing miR-20b-3p or inhibiting circ_0084927, but its expression was rescued when circ_0084927 and miR-20b-3p were both inhibited. Finally, AKT-mTOR signaling was markedly regulated by circ_0084927 and miR-20b-3p.
The expression of circ_0084927 is significantly increased in CRC and higher in advanced-stage CRC than in early-stage CRC. Moreover, circ_0084927 potentially regulates CRC migration and invasion via the miR-20b-3p/GSTM5/AKT/mTOR pathway.
Circ_0084927 could promote CRC progression and provide a new treatment strategy for CRC with metastasis.