TRMT6 is Suppressed by miR-191-5p and Functions as a Tumor Promoter in Ovarian Cancer

Abstract

Abstract Ovarian cancer has a high mortality, and RNA methylation plays a role in several cancers. Our study aimed to explore the effects of differential expression of TRMT6, an N1-methyladenosine writer, on ovarian cancer and its upstream regulatory mechanism. Preliminary bioinformatics analysis revealed that TRMT6 was differentially expressed in ovarian cancer and normal ovarian tissues. Patients with ovarian cancer and high TRMT6 expression had a poor prognosis, and the area under the receiver operating characteristic curve was 0.759. This finding suggests that TRMT6 may be used as a biomarker for ovarian cancer. We used immunohistochemistry to verify the differential expression of TRMT6 in ovarian cancer and normal ovarian tissues. The differential expression of TRMT6 in ovarian cancer cell lines A2780 and OVCAR3 was confirmed using qPCR and western blotting. CCK-8, transwell assay results suggested that overexpression of TRMT6 promoted the proliferation and migration of ovarian cancer cells, whereas overexpression of miR-191-5p reduced these effects. Results of dual-luciferase reporter gene assays indicated that TRMT6 was the target gene of miR-191-5p. In conclusion, TRMT6 promoted the proliferation and migration of ovarian cancer cells, and its upstream miR-191-5p targeted and regulated TRMT6 to reduce these effects. TRMT6 gene expression may be used as a prognostic biomarker and its regulation as a therapeutic target in ovarian cancer.