Long noncoding RNAs (IncRNAs) regulate gene expression at epigenetic, transcriptional, post-transcriptional levels and play important roles in tumorigenesis and inflammation. In order to explore the effects of IncRNAs on the malignant behavior of cervical cancer (CC) which may be involved in mechanism stimulated by inflammatory factors, we screened a differential expression profile of IncRNAs in CC cells stimulated by TNF-alpha by deep sequencing. We characterized a significantly upregulated IncRNA LOC105374902 induced by TNF-alpha. Then, we found that TNF-alpha accelerated the binding of STAT3 to the promoter region of IncRNA LOC105374902 and promoted its expression. Mechanistically, IncRNA LOC105374902 directly bond to miR-1285-3p as a competing endogenous RNA (ceRNA) to derepress RPL14; functional analysis indicated that both IncRNA LOC105374902 and RPL14 promoted migration, invasion and epithelial-mesenchymal transition (EMT) of CC cells. Taken together, TNF-alpha-induced IncRNA LOC105374902 may function as a ceRNA for miR-1285-3p to promote the expression of RPL14, promoting the migration, invasion and EMT of CC cells. These findings may provide new insights into the molecular pathogenesis of CC. (C) 2019 Elsevier Inc. All rights reserved.