Clinical and biological impact of SNAT7 in lung adenocarcinoma: implications for prognosis and treatment.

Background: Glutamine metabolism plays a crucial role in cancer cell proliferation and modulates the tumour microenvironment. High expression of glutamine transporters is associated with poor prognosis in non-small cell lung cancer. SNAT7, encoded by SLC38A7, facilitates glutamine transport from lysosomes. However, its function and clinical significance in lung adenocarcinoma remain unclear.

Materials and methods: Immunohistochemistry (IHC) was performed with samples from 373 patients with completely resected lung adenocarcinoma, and the association between SNAT7 expression, clinicopathological features, and prognosis was examined. In addition, the biological findings were investigated in lung adenocarcinoma cell lines.

Results: Based on IHC analysis, we classified patients into high (n = 226, 60.6%) and low SNAT7 expression (n = 147, 39.4%) groups. High SNAT7 expression was substantially associated with male sex, smoking status, high maximum standardised uptake value, advanced pathological stage, and pleural, lymphatic, and vascular invasion, compared to low SNAT7 expression. Patients with high SNAT7 expression demonstrated substantially worse recurrence-free survival (RFS) and overall survival rates. Multivariable analysis revealed that high SNAT7 expression was an independent prognostic factor for RFS. In addition, SLC38A7 knockdown induced a decrease in proliferation with G1 arrest in lung adenocarcinoma cell lines.

Conclusion: Our findings demonstrate that SNAT7 plays a pivotal role in promoting tumour malignancy and is significantly associated with poor prognosis in lung adenocarcinoma. These findings suggest that SNAT7 is a potential therapeutic target in lung adenocarcinoma.