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Oral squamous cell carcinoma (OSCC) is a cancer with high morbidity and mortality. Research has demonstrated that long non‑coding RNAs (lncRNAs) are critical for tumor initiation and development. In the present study, we aimed to ascertain the functions and potential mechanisms of lncRNA plasmacytoma variant translocation 1 (PVT1) in OSCC. Firstly, we found that the expression of PVT1 was increased in human OSCC tumor tissues and it was related to reduced survival of the patients. Furthermore, miR‑150‑5p expression was downregulated in OSCC tumor tissues and it was negatively related with PVT1. Moreover, GLUT‑1 protein expression was upregulated in human OSCC tumor tissues. In addition, cell proliferation capacity was measured by CCK‑8 assay and cell invasion and migration were measured by Transwell assay. PVT1 overexpression promoted cell proliferation, invasion and migration, while these effects were abrogated by PVT1 downregulation. In addition, luciferase gene reporter assay verified the miR‑150‑5p directly binds with PVT1, which regulates the biological functions of OSCC. Additionally, luciferase gene reporter assay confirmed that GLUT‑1 was a target for miR‑150‑5p. The promotion of cell proliferation, invasion and migration in LV‑PVT1‑transfected cells was eliminated following miR‑150‑5p overexpression. Finally, in vivo nude mouse xenograft model further verified that PVT1 knockdown inhibited tumor growth, formation, invasion and migration. According to the results, PVT1 is increased in human OSCC tumor tissues, and is related to the poor prognosis of human OSCC patients. We uncovered a previously unappreciated PVT1/miR‑150‑5p/GLUT‑1 signaling axis that promotes cell proliferation, invasion, migration and inhibits apoptosis in OSCC cell lines and in vivo, which suggests that this axis could be a target for the treatment of OSCC.

oncology reports

Long noncoding RNA PVT1 promotes tumor cell proliferation, invasion, migration and inhibits apoptosis in oral squamous cell carcinoma by regulating miR‑150‑5p/GLUT‑1