Abstract
Cervical cancer (CC) is the most common gynecological malignant tumor in the world. Long non-coding RNA (lncRNAs) plays an important role in cell activities of various cancers including CC. This study aims to reveal the biological function of FLVCR1-AS1 in CC and clarify its possible mechanism of action. The findings suggest that the expression of FLVCR1-AS1 was elevated in CC tissues and cell lines, and that high expression of FLVCR1-AS1 was associated with poor prognosis of CC patients. In addition, knockdown of FLVCR1-AS1 could inhibit the proliferation and migration, invasion and epithelial-mesenchymal transformation (EMT) of CC cells, as well as accelerating apoptosis, to inhibit the development of CC. In addition, via the dual-luciferase reporting assay and RIP assay were confirmed that FLVCR1-AS1 acted as a competitive endogenous RNA to inhibit the expression of microRNA (miR)-23a-5p, and miR-23a-5p targeted the 3'-untranslated region site of Solute carrier family 7 member 11 (SLC7A11) and negatively regulated the expression of SLC7A11. Functional rescue experiments showed that miR-23a-5p inhibitors reversed the inhibitory effect of FLVCR1-AS1-silencing on proliferation, EMT, migration and invasion, and the promoting impact of apoptosis of CC cells. In addition, SLC7A11 rescued the effect of miR-23a-5p overexpression on progression of CC cells. In conclusion, FLVCR1-AS1 is involved in the malignant phenotype of CC cells through miR-23a-5p/SLC7A11 axis, which may provide a beneficial direction for the treatment of CC.