LINC00657 promotes malignant progression of oral squamous cell carcinoma via regulating microRNA-150.

Abstract

Previous studies have shown that LINC00657 is a cancer-promoting gene. However, the role of LINC00657 in oral squamous cell carcinoma (OSCC) has not been reported. This study was designed to investigate the role of LINC00657 in OSCC and its regulatory mechanism. Quantitative Real Time-Polymerase Chain Reaction (qPCR) was used to detect the levels of LINC00657 and microRNA-150 in 32 pairs of OSCC tissues and normal ones, and the correlation between LINC00657 and clinical indicators and OSCC patient's prognosis was analyzed. qRT-PCR further verified the levels of LINC00657 and microRNA-150 in OSCC cells. In addition, LINC00657 overexpression and knockdown models were constructed using lentivirus in OSCC cell lines Fadu and Tca8113, and Cell Counting Kit-8 (CCK-8), plate clone experiment, and 5-Ethynyl-2'-deoxyuridine (EdU) assay were carried out to evaluate the influence of LINC00657 on the biological functions of OSCC cells. Further, Luciferase reporter gene and recovery experiments were used to explore its potential mechanism. qRT-PCR showed that LINC00657 expression in OSCC tissue specimens was increased in comparison to normal ones. Patients with high LINC00657 expression had higher pathological staging and lower overall survival. Besides, the cell proliferation ability of the LINC00657 silencing group was remarkably decreased, while the opposite result was observed in LINC00657 overexpression group. Subsequently, qRT-PCR demonstrated a significant decrease in microRNA-150 expression in OSCC cell lines and tissues and a negative correlation with LINC00657. Luciferase assay demonstrated that LINC00657 could be targeted by microRNA-150 in certain binding sites. In addition, cell reverse experiment also confirmed that LINC00657 and microRNA-150 can be mutually regulated, thereby jointly modulating the malignant progression of OSCC. LINC00657, remarkably upregulated in OSCC tissues, showed a close association with the poor prognosis of OSCC patients. Additionally, it may accelerate the malignant progression of OSCC via regulating microRNA-150.