Exosome long non-coding RNA SOX2-OT contributes to ovarian cancer malignant progression by miR-181b-5p/SCD1 signaling

Ovarian cancer is a common gynecologic cancer with increased mortality and morbidity. Exosome-delivered long non-coding RNAs have been well found in cancer development. However, the function of exosomal SOX2-OT in ovarian cancer development is still unreported. In the present study, we were interested in the investigation of the effect of exosomal SOX2-OT during ovarian cancer pathogenesis. Significantly, we revealed that the 50X2-OT expression levels were up-regulated in the ovarian cancer patients' plasma exosomes. The depletion of exosomal 50X2-OT inhibited migration, invasion, and proliferation and induced apoptosis in ovarian cancer cells. In mechanical exploration, 50X2-OT could sponge miR-181b-5p, and miR-181b-5p was able to target SCD1 in the ovarian cancer cells. The SCD1 overexpression and miR-181b-5p inhibitor could reverse exosomal SOX2-OT-mediated ovarian cancer progression. Functionally, the depletion of exosomal 50X2-OT significantly reduced tumor growth of ovarian cancer cells in vivo. In summary, we concluded that exosomal 50X2-OT enhanced ovarian cancer malignant phenotypes by miR-181b-5p/SCD1 axis. Our finding presents novel insights into the mechanism by which exosomal IncRNA 50X2-OT promotes ovarian cancer progression. 50X2-OT, miR-181b-5p, and SCD1 may serve as potential targets for the treatment of ovarian cancer.

Automated summary

This study revealed the role of exosomal SOX2-OT in enhancing ovarian cancer malignant phenotypes through the miR-181b-5p/SCD1 axis. Exosomal 50X2-OT, miR-181b-5p, and SCD1 may serve as potential targets for the treatment of ovarian cancer.