摘要
Long non-coding RNAs（lncRNAs） have been reported to be of great importance in tumorigenesis and progression of a variety of cancers. However, the role of lncRNAs in ovarian cancer（OC） remains largely unknown. In the present study, we identified a novel lncRNA, LOC100288181（named as Lnc-OC1）, which acted as a key regulator in the development and progression of OC. The combined Gene Expression Omnibus（GEO） database analysis revealed that Lnc-OC1 was significantly upregulated in OC tissues and Kaplan-Meier survival analysis confirmed that high Lnc-OC1 expression was associated with poor prognosis of OC patients. Importantly, we also demonstrated that knockdown of Lnc-OC1 suppressed cell proliferation, colony formation, invasion and migration in vitro and inhibited tumorigenicity in vivo.Mechanistically, Lnc-OC1 repressed the expression of endogenous miR-34 a and miR-34 c as a sponge and vice versa. Moreover, rescue experiments demonstrated that the oncogenic function of Lnc-OC1 at least partially depended on suppressing miR-34 a and miR-34 c. In conclusion, our results suggest that the LncOC1-miR-34 a/34 c axis may play a pivotal role in OC, and may serve as a potential diagnostic biomarker and a powerful therapeutic target for OC.
Long non-coding RNAs（lncRNAs） have been reported to be of great importance in tumorigenesis and progression of a variety of cancers. However, the role of lncRNAs in ovarian cancer（OC） remains largely unknown. In the present study, we identified a novel lncRNA, LOC100288181（named as Lnc-OC1）, which acted as a key regulator in the development and progression of OC. The combined Gene Expression Omnibus（GEO） database analysis revealed that Lnc-OC1 was significantly upregulated in OC tissues and Kaplan-Meier survival analysis confirmed that high Lnc-OC1 expression was associated with poor prognosis of OC patients. Importantly, we also demonstrated that knockdown of Lnc-OC1 suppressed cell proliferation, colony formation, invasion and migration in vitro and inhibited tumorigenicity in vivo.Mechanistically, Lnc-OC1 repressed the expression of endogenous miR-34 a and miR-34 c as a sponge and vice versa. Moreover, rescue experiments demonstrated that the oncogenic function of Lnc-OC1 at least partially depended on suppressing miR-34 a and miR-34 c. In conclusion, our results suggest that the LncOC1-miR-34 a/34 c axis may play a pivotal role in OC, and may serve as a potential diagnostic biomarker and a powerful therapeutic target for OC.
基金
was supported by the China Postdoctoral Science Foundation Grant(No.2015M581292)
the National Natural Science Foundation of China(No.81302896)
the Zhejiang Provincial Public Welfare Projects(No.2016C37056)
