TNF-α-induced lncRNA LOC105374902 promotes the malignant behavior of cervical cancer cells by acting as a sponge of miR-1285-3p.

Biochem Biophys Res Commun

Tianjin Life Science Research Center, Tianjin Key Laboratory of Inflammation Biology, Collaborative Innovation Center of Tianjin for Medical Epigenetics, Department of Pathogen Biology, School of Basic Medical Sciences, Tianjin Medical University, Tianjin, China. Electronic address:

Published: May 2019

Long noncoding RNAs (lncRNAs) regulate gene expression at epigenetic, transcriptional, post-transcriptional levels and play important roles in tumorigenesis and inflammation. In order to explore the effects of lncRNAs 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 lncRNAs in CC cells stimulated by TNF-α by deep sequencing. We characterized a significantly upregulated lncRNA LOC105374902 induced by TNF-α. Then, we found that TNF-α accelerated the binding of STAT3 to the promoter region of lncRNA LOC105374902 and promoted its expression. Mechanistically, lncRNA LOC105374902 directly bond to miR-1285-3p as a competing endogenous RNA (ceRNA) to derepress RPL14; functional analysis indicated that both lncRNA LOC105374902 and RPL14 promoted migration, invasion and epithelial-mesenchymal transition (EMT) of CC cells. Taken together, TNF-α-induced lncRNA 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.

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http://dx.doi.org/10.1016/j.bbrc.2019.03.079DOI Listing

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