Investigating resistin like beta (RETNLB) as a tumor promoter for oral squamous cell carcinoma.

BACKGROUND

Oral cavity cancer ranks the sixth most common malignancy worldwide, of which oral squamous cell carcinoma is the predominant type. This study aimed to investigate the function and the underlying mechanism of resistin like beta (RETNLB) in oral squamous cell carcinoma.

METHODS

The data of oral squamous cell carcinoma samples from The Cancer Genome Atlas database was used to examine RETNLB expression and assess its correlation with the clinical outcomes. Biological functions of RETNLB on the growth, invasion and migration of cells were determined by cell counting kit 8, clonogenic growth, and Transwell assays. Gene set enrichment analysis was utilized to identify the important gene sets associated with RETNLB expression, which was further confirmed by western blot.

RESULTS

We found that RETNLB was upregulated in oral squamous cell carcinoma tissues and cells. High expression of RETNLB was closely linked to age and pathological tumor, and significantly related to poor survival of oral squamous cell carcinoma patients. Further functional experiments showed that knockdown of RETNLB significantly reduced the viability, mobility and invasiveness of cells. Moreover, gene set enrichment analysis suggested that Toll-like receptor signaling pathway was significantly correlated with high RETNLB expression. Further western blot analysis verified that silencing RETNLB could notably suppress the protein levels of Toll-like receptor 2, Toll-like receptor 4 and phosphor- extracellular signal-regulated kinase.

CONCLUSIONS

These results suggested that downregulation of RETNLB may restrain the progression of oral squamous cell carcinoma by inactivating TLR/2/4/ERK pathway.