Co-upregulation of and its host gene lncRNA in oral squamous cell carcinoma.

BACKGROUND/PURPOSE: Several long non-coding RNAs (lncRNAs) harbor miRNA in their genome. MIR31HG harbors miR-31 in its intron and it is speculated that they are co-expressed in tumors. This study addressed whether frequent miR-31 and MIR31HG co-upregulation occurred in oral squamous cell carcinoma (OSCC) and its clinical implications.

MATERIALS AND METHODS

Microarray was performed to retrieve dis-regulated lncRNAs from tissue sample. The ectopic gene expression was carried out to specify the phenotypic influences of selected lncRNA screened from bioinformatic algorithms. The expression of and in tissues or scrapped samples was analyzed using qRT-PCR. The implications of gene expression as related to metastasis or survival were further dissected.

RESULTS

Microarray identified disrupted transcripts including and other 152 lncRNAs aberrantly expressed in OSCC tissues. algorithms annotated an eminent involvement of aberrant transcripts in the regulation of cell cycle, extracellular modulation, adhesion, and wound healing. The enhancement of proliferation, wound healing, invasion and anchorage-independent colony formation mediated by was ascertained by ectopic expression in OECM1 cells. Besides, co-upregulation of and was conspicuous in OSCC tissues. High expression of and designated a trend of worse OSCC prognosis. Interestingly, high expression defined a very poor survival in stage IV diseases. By contrast, high expression predicted nodal metastasis in stage I-III diseases.

CONCLUSION

Assessment of miR-31 and MIR31HG expression in OSCC may enable the prognostic prediction. The candidate lncRNAs isolated from this work can be further validated as crucial factors contributing to OSCC pathogenesis.