LINC00525 promotes tumour growth and epithelial-mesenchymal transition as an oncogene in oral squamous cell carcinoma

Objective Oral squamous cell carcinoma (OSCC) is the most common malignant tumour in the oral cavity. OSCC is aggressive and prone to metastasis; it is associated with high mortality and short survival. In this study, we investigated the function of the long non-coding RNA LINC00525 in OSCC progression and the molecular mechanisms through in vitro and in vivo experiments.Materials and Methods CCK8 assay was used to detect the effect of LINC00525 on cell viability; transwell migration and invasion assays and scratch assay were used to examine the role of LINC00525 in cell migration and invasion. Flow cytometry, RT-PCR and western blot were used to detect apoptosis indexes. Tumorigenic effects were investigated using mouse xenograft tumour models.Results LINC00525 was associated with OSCC survival and prognosis. LINC00525 knockdown decreased cell viability and epithelial-mesenchymal transition (EMT) properties and increased apoptosis and also shortened the cell cycle of OSCC cells in vitro. The downregulation of LINC00525 reduced the growth of OSCC tumour in vivo. LINC00525 can regulate OSCC cells via the apoptotic signalling pathway.Conclusion Our results indicate that LINC00525 exhibits oncogenic functions in OSCC. LINC00525 may be a new promising and potential target for the treatment of OSCC.

Automated summary

In this study, the function of the long non-coding RNA LINC00525 in the progression of oral squamous cell carcinoma (OSCC) was investigated through in vitro and in vivo experiments. The results showed that LINC00525 was associated with OSCC survival and prognosis. Knockdown of LINC00525 decreased cell viability, migration and invasion properties, and increased apoptosis in OSCC cells. In vivo experiments also demonstrated that downregulation of LINC00525 reduced OSCC tumour growth. Therefore, LINC00525 may serve as a potential target for the treatment of OSCC.