Mechanism underlying long non-coding RNA ILF3-AS1-mediated inhibition of cervical cancer cell proliferation, invasion and migration, and promotion of apoptosis

Long non-coding RNA ILF3 divergent transcript (ILF3-AS1) displays a tumor-suppressing effect. StarBase predicted that the potential target microRNA (miR) of ILF3-AS1 was miR-454-3p; therefore, the present study investigated the effect of ILF3-AS1 and its target miR-454-3p on cervical cancer (CC). Gene Expression Profiling Interactive Analysis was used to predict the expression of ILF3-AS1 in CC and the overall survival rate of patients. The present study demonstrated that ILF3-AS1 expression was significantly downregulated in human CC tissues and cells compared with adjacent tissues (ANTs) and normal cervical epithelial cells (NCEs), respectively. Patients with CC with high ILF3-AS1 expression displayed higher survival rates compared with patients with low ILF3-AS1 expression. Cell viability, apoptosis, migration and invasion were detected by performing Cell Counting Kit-8, flow cytometry, wound healing and Transwell assays, respectively. Compared with the negative control (NC) group, ILF3-AS1 overexpression significantly inhibited CC cell viability and migration, but significantly increased CC cell apoptosis. Moreover, ILF3-AS1 overexpression significantly upregulated E-Cadherin expression levels, but significantly downregulated N-Cadherin and snail family transcriptional repressor 1 expression levels compared with the NC group. miR-454-3p expression was negatively correlated with ILF3-AS1, and highly expressed in CC tissues and cells compared with ANTs and NCEs, respectively. PTEN, which was predicted and verified as the target gene for miR-454-3p, was significantly downregulated in CC tissues and cells compared with ANTs and NCEs, respectively. ILF3-AS1 expression was positively correlated with PTEN expression, and ILF3-AS1 overexpression partially reversed the inhibitory effect of miR-454-3p on PTEN expression. In conclusion, the present study indicated that ILF3-AS1 inhibited CC cell proliferation and migration, and promoted CC cell apoptosis by inhibiting epithelial-mesenchymal transition, and ILF3-AS1 overexpression partially reversed the inhibitory effect of miR-454-3p on PTEN expression.