Long noncoding RNAs have been demonstrated to contribute to the development and progression of various cancers. However, the underlying regulatory mechanisms of KCNQ1OT1 in tumorigenesis of maxillary sinus squamous cell carcinoma (MSSCC) remain unknown. Herein, we found that KCNQ1OT1 expression was markedly upregulated in MSSCC tissues and MSSCC cell line (IMC-3) by using quantitative reverse transcription-polymerase chain reaction. Loss-of-function experiments revealed that the deletion of KCNQ1OT1 inhibited cell proliferation, migration, and invasion. Moreover, we confirmed KCNQ1OT1 could directly interact with miR-204 by bioinformatic prediction and dual luciferase assay, and miR-204 inhibitor markedly reversed MSSCC tumor phenotypes induced by shKCNQ1OT1. Finally, we demonstrated that KCNQ1OT1/miR-204 facilitated MSSCC progression by regulating Eph receptor A7 (EphA7). Taken together, these results revealed a novel regulatory mechanism KCNQ1OT1/miR-204/EphA7 axis, which could provide a new understanding of MSSCC tumorigenesis and develop potential targets for MSSCC therapy.
Keywords: EphA7; lncRNA KCNQ1OT1; maxillary sinus squamous cell carcinoma (MSSCC); miR-204.
© 2019 Wiley Periodicals, Inc.