A long non-coding RNA (lncRNA) called prostate cancer-associated non-coding RNA 1 (PRNCR1) serves crucial roles in the aggressive phenotypes of colorectal cancer and non-small cell lung cancer. However, there is little research on the expression profile, clinical value and detailed functions of PRNCR1 in tongue squamous cell carcinoma (TScc). The aim of the present study was to determine PRNCR1 expression in TScc and to examine the involvement of PRNCR1 in TScc progression. The molecular mechanisms behind the oncogenic effects of PRNCR1 in TScc cells were also investigated. PRNCR1 was revealed to be upregulated in TScc tumors and cell lines. The high PRNCR1 expression showed a significant correlation with tumor size, clinical stage, lymph node metastasis, and shorter overall survival times among patients with TScc. A PRNCR1-knockdown reduced TScc cell proliferation, migration and invasion, and increased apoptosis in vitro. Additionally, the PRNCR1-knockdown slowed down in vivo tumor growth of TScc cells. With regards to the mechanism, PRNCR1 acted as a competing endogenous RNA on microRNA-944 (miR-944) in TScc cells, and the effects of the PRNCR1-knockdown were reversed by an miR-944-knockdown. HOXB5 was validated as a direct target gene of miR-944 in TScc cells, and HOXB5 expression was found to be positively regulated by PRNCR1. Furthermore, resumption of HOXB5 expression reversed the tumor-suppressive actions of miR-944 in TScc cells. In conclusion, PRNCR1 acts as an oncogenic lncRNA in TScc through the upregulation of HOXB5 by sponging miR-944, thereby indicating a potential therapeutic target in TScc.

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Comparative assessment of autogenous cancellous bone graft and bovine-derived demineralized bone matrix for secondary alveolar bone grafting in patients with unilateral cleft lip and palate.