A novel oncogene trigger transposable element derived-1 promotes oral squamous cell carcinoma progression via evoking immune inhibition

Oral squamous cell carcinoma (OSCC) is one of the most common head and neck squamous cell carcinomas (HNSCC) globally. Its incidence rate is rapidly increasing, and its 5-year survival rate remains at 50%, despite advances in medical science. Trigger transposable element-derived 1 (TIGD1) has been found to be upregulated in various cancer types. However, its biological function in OSCC requires further investigation. We searched the Cancer Genome Atlas database using CIBERSORT and TIMER 2.0 to predict the significance of TIGD1 and evaluate its effect on immune cell infiltration. Gene set enrichment analysis was performed to determine the biological functions of TIGD1. Gain/loss of function techniques were used to explore the biological behavior of TIGD1 in Cal27 and HSC4 cells. Finally, flow cytometry was used to detect dendritic cell markers in an OSCC and dendritic cell co-culture model. Our results show that TIGD1 is upregulated significantly in OSCC and is closely associated with tumor progression and prognosis. TIGD1 functions as an oncogene by increasing cells proliferation, inhibiting apoptosis, promoting cell invasion and migration. TIGD1 is also involved in tumor immune cell infiltration. Its overexpression can inhibit dendritic cell maturation, leading to immune suppression and tumor progression. High TIGD1 expression, which promotes OSCC progression, might be related to decreased dendritic cell maturation and activation. These findings suggest that TIGD1-specific small interfering RNA synthesized in vitro could be a new target for OSCC immunotherapy.

Automated summary

Oral squamous cell carcinoma (OSCC) is a common type of head and neck cancer that is rapidly increasing with a low survival rate. The upregulation of TIGD1 in OSCC and its effects on tumor progression and immune cell infiltration were investigated. TIGD1 was found to function as an oncogene, promoting cell proliferation, inhibiting apoptosis, and enhancing cell invasion and migration. It was also involved in inhibiting dendritic cell maturation, leading to immune suppression and tumor progression. These findings suggest that TIGD1 could be a potential target for immunotherapy in OSCC.