Department of Obstetrics, People's Hospital of Rizhao, Rizhao, China.
Department of Health Emergency Office, Rizhao Center for Disease Control and Prevention, Rizhao, China.
Aging (Albany NY). 2021 Oct 24;13(20):23726-23738. doi: 10.18632/aging.203645.
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 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.
卵巢癌是一种常见的妇科癌症,死亡率和发病率都有所增加。外泌体携带的长非编码 RNA 已被广泛发现与癌症的发生发展有关。然而,外泌体 SOX2-OT 在卵巢癌发展中的作用尚不清楚。在本研究中,我们对研究外泌体 SOX2-OT 在卵巢癌发病机制中的作用很感兴趣。研究结果表明,卵巢癌患者血浆外泌体中的 SOX2-OT 表达水平上调。外泌体 SOX2-OT 的耗竭抑制了卵巢癌细胞的迁移、侵袭和增殖,并诱导其凋亡。在机制探索中,我们发现 SOX2-OT 可以海绵吸附 miR-181b-5p,而 miR-181b-5p 能够靶向卵巢癌细胞中的 SCD1。SCD1 的过表达和 miR-181b-5p 抑制剂可以逆转外泌体 SOX2-OT 介导的卵巢癌细胞进展。功能上,外泌体 SOX2-OT 的耗竭显著降低了卵巢癌细胞的肿瘤生长。综上所述,我们得出结论,外泌体 SOX2-OT 通过 miR-181b-5p/SCD1 轴增强了卵巢癌的恶性表型。我们的发现为外泌体 lncRNA SOX2-OT 促进卵巢癌进展的机制提供了新的见解。SOX2-OT、miR-181b-5p 和 SCD1 可能成为治疗卵巢癌的潜在靶点。