Silencing of long non-coding RNA LINC00958 inhibits head and neck squamous cell carcinoma progression and AKT/mTOR signaling pathway by targeting miR-106a-5p.

OBJECTIVE

The long non-coding RNA LINC00958 acts as an oncogenic regulator in many human tumors. In this study, we aimed to investigate the role and potential molecular biological mechanisms of LINC00958 in head and neck squamous cell carcinoma (HNSCC).

MATERIALS AND METHODS

Aberrantly expressed LINC00958 was screened out of TCGA database. The quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) was used to determine LINC00958 and miR-106a-5p expression. Cellular biological behaviors were investigated using CCK-8, colony formation, wound healing and transwell assays. Xenograft mouse models were established to determine the role of LINC00958 in HNSCC growth in vivo. The interaction between LINC00958 and miR-106a-5p was validated by Dual-Luciferase reporter gene assay. Additionally, the underlying pathways affected by LINC00958 were measured by Western blot.

RESULTS

LINC00958 expression was upregulated in HNSCC tissues and cells. High LINC00958 level was correlated with the poor prognosis of HNSCC patients. Functional assays showed that the knockdown of LINC00958 inhibited HNSCC malignant phenotypes in vitro and in vivo. Mechanistically, miR-106a-5p was a potential target of LINC00958, and its expression was negatively regulated by LINC00958 in HNSCC. LINC00958 could activate AKT/mTOR signaling pathway, which was mediated by miR-106a-5p.

CONCLUSIONS

Taken together, our results suggest that LINC00958 acts as an oncogenic role in HNSCC and activates AKT/mTOR signaling pathway by sponging miR-106a-5p. LINC00958 may serve as a potential target for HNSCC diagnosis and treatment.