Abstract
BACKGROUND: Long non-coding RAN five prime to Xist (LncRNA FTX) has been revealed to be a cancer-related lncRNA and implicated in the progression of colorectal cancer (CRC). Besides, miR-192-5p (miR-192) or eukaryotic initiation factor 5A2 (EIF5A2) also was identified to link with the tumorigenesis of CRC. Here, we further explored the function of FTX and the regulatory relationship among FTX, miR-192 and EIF5A2 in CRC progression. METHODS: Levels of FTX, miR-192-5p and EIF5A2 were detected by quantitative real-time polymerase chain reaction (qRT-PCR) or Western blot, respectively. Cell proliferation, apoptosis, migration and invasion were analyzed using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, flow cytometry or transwell assay, respectively. The interaction between miR-192-5p and FTX or EIF5A2 was confirmed by dual-luciferase reporter and pull-down assay. Murine xenograft model was established using LoVo cells transfected with sh-FTX. RESULTS: FTX was up-regulated in CRC tissues and cell lines, knockdown of FTX inhibited CRC cell proliferation, migration and invasion in vitro as well as suppressed CRC tumor growth in vivo. FTX was confirmed to directly bind to miR-192-5p and negatively regulated miR-192-5p expression in CRC cells. Besides that overexpressed FTX positively modulated EIF5A2, a direct target of miR-192-5p, via miR-192-5p in CRC cells. Importantly, the inhibitory activities on CRC progression mediated by FTX deletion were reversed miR-192-5p down-regulation or EIF5A2 up-regulation. CONCLUSION: LncRNA FTX functioned as an oncogene to contribute to CRC progression by regulating miR-192-5p/EIF5A2 axis, providing a novel insight into the pathogenesis of CRC and a promising therapeutic target for CRC treatment.