Purpose: Long intergenic non-protein-coding RNA 00466 (LINC00466 ) promotes lung adenocarcinoma progression. Nonetheless, the expression and precise roles of LINC00466  in tongue squamous cell carcinoma (TSCC) remains uncertain and warrant further investigation. Hence, the present study aimed to examine the LINC00466 effects on the aggressive TSCC cell characteristics and to elucidate the potential underlying mechanisms.
Methods: First, LINC00466  expression in TSCC was determined by reverse transcription-quantitative PCR. Subsequently, cell proliferation, apoptosis, migration, and invasion in vitro, as well as tumor growth in vivo were assessed to examine the LINC00466  effects on TSCC cells.
Results: LINC00466  was upregulated in TSCC. This upregulation was notably associated with shorter overall TSCC patient survival. In vitro experiments indicated that LINC00466  depletion suppressed TSCC cell proliferation, migration and invasion, and promoted apoptosis. An in vivo experiment revealed that LINC00466  downregulation attenuated TSCC tumor growth in vivo. Mechanistic analysis revealed that LINC00466  functions as a microRNA-493 (miR-493) molecular sponge, a miRNA that targets high-mobility group AT-hook 2 (HMGA2 ) mRNA. LINC00466  upregulated HMGA2 in TSCC cells, and this phenomenon was regulated by the miR-493 sponge. Rescue experiments revealed a decrease in the miR-493/HMGA2 axis output, partially reversing the effects of LINC00466  downregulation on aggressive TSCC cell behavior.
Conclusion: These findings demonstrate that LINC00466  promotes TSCC cell oncogenicity in vitro and in vivo by upregulating the miR-493/HMGA2 axis output. These results may provide a new perspective and new insight into the molecular mechanisms of TSCC.
Keywords: long intergenic non-protein-coding RNA 00466, tongue squamous cell carcinoma pathogenesis, targeted therapy