Long noncoding RNA UFC1 is activated by E2F1 and exerts oncogenic properties by functioning as a ceRNA of FOXP3.

Cervical cancer is one of the most common gynecologic cancers around the world. Long noncoding RNAs (lncRNAs) are considered to be important regulators of some biological processes. Recently, it has been reported that linc-UFC1 is a putative oncogene in some cancers. However, the functional roles of linc-UFC1 have not been investigated in cervical cancer. Here, it was demonstrated that linc-UFC1 expression was significantly increased in cervical cancer tissues, and its overexpression was associated with the poor survival of patients with cervical cancer. Loss-of-function assays indicated that linc-UFC1 exerted as an oncogene because it promoted the growth and metastasis of cervical cancer cells in vitro and in vivo. Mechanistic investigations revealed that linc-UFC1 upregulated FOXP3 expression through competitively binding miR-34a. Finally, luciferase reporter and chromatin immunoprecipitation (ChIP) assays provided evidence that E2F1 could directly bind to the linc-UFC1 promoter region and enhance its transcription. Taken together, our findings indicate that the linc-UFC1 expression signature may serve as a novel biomarker for the diagnosis and prognosis of cervical cancer, and it is also highlighted that the E2F1-linc-UFC1/miR-34a/FOXP3 axis may be a potentially therapeutic target of cervical cancer.