Abstract
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 SOX2-OT expression levels were up-regulated in the ovarian cancer patients’ plasma exosomes. The depletion of exosomal SOX2-OT inhibited migration, invasion, and proliferation and induced apoptosis in ovarian cancer cells. In mechanical exploration, SOX2-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 SOX2-OT significantly reduced tumor growth of ovarian cancer cells in vivo. In summary, we concluded that exosomal SOX2-OT enhanced ovarian cancer malignant phenotypes by miR-181b-5p/SCD1 axis. Our finding presents novel insights into the mechanism by which exosomal lncRNA SOX2-OT promotes ovarian cancer progression. SOX2-OT, miR-181b-5p, and SCD1 may serve as potential targets for the treatment of ovarian cancer.
Highlights
Ovarian cancer serves as the primary reason for women cancer-related mortality in all gynecologic tumors [1]
We performed the lncRNA profiling in the exosomes from ovarian cancer patients (n = 5) and normal samples (n = 5) and identified the elevated expression of SOX2-OT in the exosomes from ovarian cancer patients compared with normal samples (Figure 1A)
To assess the potential correlation of exosomal SOX2-OT with the ovarian cancer progression, we analyzed their expression in the plasma exosome of ovarian cancer patients
Summary
Ovarian cancer serves as the primary reason for women cancer-related mortality in all gynecologic tumors [1]. Despite therapies have been advanced, treatments are limited because of drug-resistance [2]. The diagnosis normally occurs at the more advanced stage in ovarian cancer patients [3]. Current treatment is not available to cure ovarian cancer, and 5-year survival incidence maintains at 45% [4]. Understanding the molecular mechanism of ovarian cancer progression will be helpful for the improvement of therapeutic strategies for ovarian cancer [5,6,7]. The investigation of the molecular mechanism of ovarian cancer development is still limited
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