Study on the role and mechanism of TMED2 in oral squamous cell carcinoma.

PURPOSE

This study investigated TMED2 expression in oral squamous cell carcinoma (OSCC) and its effects on SCC9 cell behaviors, including proliferation, migration, invasion, and autophagy, to support OSCC diagnosis and treatment.

METHODS

TMED2 expression was analyzed in TCGA and GEO databases, and protein levels in OSCC tissues were examined via HE staining and tissue microarrays. SCC9 cells, with high TMED2 expression, were used to assess TMED2's effects on cell proliferation, invasion, and cell cycle. TMED2 knockdown was performed with lentiviral vectors, and RT-PCR and Western blotting explored the autophagy and AKT/mTOR pathways. Tumor growth was tested in TMED2 knockdown and control cells in nude mice.

RESULTS

TMED2 was highly expressed in OSCC, correlating with poor prognosis. Knockdown of TMED2 significantly reduced SCC9 cell proliferation, migration, and invasion, induced G0/G1 cell cycle arrest, reduced AKT/mTOR pathway activity, and increased autophagy, prolonging survival in tumor-bearing mice.

CONCLUSION

TMED2 is upregulated in OSCC, correlates with poor prognosis, and regulates cell proliferation, invasion, and autophagy, indicating it as a potential therapeutic target.