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Long non-coding RNAs (lncRNAs) have been wildly verified to modulate multiple tumorigenesis, especially nasopharyngeal carcinoma (NPC). In present study, we aim to investigate the role of lncRNA FOXD2-AS1 in the NPC carcinogenesis. It was indicated that FOXD2-AS1 was markedly increased in NPC tissues and cells in comparison to their corresponding controls. Moreover, the aberrant overexpression of FOXD2-AS1 indicated the poor prognosis of NPC patients. Silence of FOXD2-AS1 was able to repress NPC cell growth in vitro while overexpression of FOXD2-AS1 inversed this process. Moreover, in vivo tumor xenografts were established using CNE-1/SUNE-1 cells to investigate the function of FOXD2-AS1 in NSCLC tumorigenesis. Rescue assay was performed to further confirm that FOXD2-AS1 contributed to NPC progression by regulating miR-363-5p/S100A1 signal pathway. Taken together, our study discovered the oncogenic role of FOXD2-AS1 in clinical specimens and cellular experiments, showing the potential FOXD2-AS1/miR-363-5p/S100A1 pathway. This results and findings provide a novel insight for NPC tumorigenesis.
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| http://dx.doi.org/10.1016/j.gene.2017.12.026 | DOI Listing |
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