TMPO‐AS1 promotes cervical cancer progression by upregulating RAB14 via sponging miR‐577

Abstract Background Accumulating evidence has shown that long non‐coding RNAs play a key role in cancer initiation and development. However, the effect of TMPO antisense RNA 1 (TMPO‐AS1) on the progression of cervical cancer (CC) remains to be determined. Methods The mRNA expression of TMPO‐AS1, miR‐577 and RAB14 was measured by a quantitative reverse transcriptase‐polymerase chain reaction. The protein level of RAB14 was detected by western blotting. The function of TMPO‐AS1 in CC was measured via Cell Counting Kit‐8, 5‐ethynyl‐2′‐deoxyuridine and transwell assays, as well as by flow cytometry analysis. Nuclear‐cytoplasmic fractionation and RNA‐fluorescence in situ hybridization validated the subcellular position of TMPO‐AS1. An interaction between miR‐577 and TMPO‐AS1 or RAB14 was confirmed by luciferase reporter, RNA pull‐down and RNA immunoprecipitation assays. Results TMPO‐AS1 was highly expressed in CC. In addition, TMPO‐AS1 knockdown inhibited proliferation and migration, and also induced apoptosis. TMPO‐AS1 located in the cytoplasm and promoted RAB14 expression by absorbing miR‐577. RAB14 overexpression or miR‐577 knockdown restored the suppressing effect of TMPO‐AS1 knockdown on the biological behavior of CC cells. Conclusions The present study has revealed a novel TMPO‐AS1/miR‐577/RAB14 regulatory axis in the pathogenesis of CC, highlighting TMPO‐AS1 as a promising therapeutic target for CC patients.