Cervical cancer has been one of the most common cancer in women worldwide. However, the detailed mechanism underlying circMTO1-regulated cervical cancer remains unclear.

RT-qPCR and westernblot were used to examine genes expression levels. Wound healing assay and transwell invasion assay were utilized to probe migration and invasion abilities of cervical cancer cells. In addition, cell viability and apoptosis were measured by MTT and TUNEL assay, respectively. Finally, we employed bioinformatic approach to analyze gene expression levels in clinical cervical cancer tissues.

circMTO1 was shown to be greatly upregulated in cervical cancer cell lines and tumors. circMTO1 directly interacts with miR-6893. miR-6893 could restore circMTO1-regulated migration, invasion and chemoresistance of cervical cancer cells. Furthermore, we identified S100A1 as downstream effector for circMTO1/miR-6893-induced tumorigenesis of cervical cancer cells. Besides, westernblot analyses demonstrated that circMTO1 and miR-6893 inhibitor enhanced Beclin1 expression and downregulated p62 level. We found that autophagy inhibitor 3-MA could revert cell viability and apoptosis of HeLa regulated by circMTO1 and miR-6893 inhibitor. More importantly, the bioinformatic results showed the dysregulated expression patterns of circMTO1, miR-6893 and S100A1 in human clinical cervical cancer tissues.

In summary, we reveal, for the first time, a novel mechanism of circMTO1/miR-6893 in tumorigenesis and chemoresistance of cervical cancer. Our findings support the notion of developing the new therapies and biomarkers by targeting circMTO1 for cervical cancer.