LINC00961 suppresses cell proliferation and induces cell apoptosis in oral squamous cell carcinoma.

Abstract

Oral squamous cell carcinoma (OSCC) is still one of the most frequent neck and head malignancies and is one of the most common cancers in the world. The main purpose of this research was to illustrate the functional role of LINC00961 in OSCC and provide novel insight of biomarkers and therapeutic strategies in OSCC. The relative expression level of LINC00961 was evaluated by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). Cell counting kit-8 (CCK-8) assay was involved for determining the ability of cell proliferation. Flow cytometric analysis was performed to detect the cell cycle and cell apoptosis. Expressions of AKT, p-AKT, BCL2, Bax protein levels were detected in Western blotting. Transfected cells were used to perform tumor xenograft formation assay. Low-expression of LINC00961 was detected in both OSCC tissues and cell lines. Through CCK-8 assay and flow cytometric analysis, we validated that up-regulated LINC00961 suppressed cell proliferation and promoted cell apoptosis in OSCC. Besides, over-expressed LINC00961 suppressed PI3K/AKT signaling pathways. In tumor xenograft formation assay, over-expressed LINC00961 inhibited tumor formation. Our research verified that LINC00961 functioned as a tumor suppressor in OSCC. Regulation of PI3K/AKT might be the underlying mechanism of the tumor suppressor role of LINC00961. The current study might bring a novel insight of biomarkers and therapeutic strategies in OSCC.