SLC38A9 Expression Correlates with Prognosis in Pancreatic Cancer: Implications for Survival and Tumor Progression

This study aims to investigate the expression level of SLC38A9 (solute carrier family 38 member 9) in pancreatic cancer and its impact on patient prognosis. Immunohistochemical analysis was performed on the pancreatic cancer clinical tissue microarray HPanAde170Sur01, which includes 99 pancreatic cancer tissues and 71 adjacent non-tumor tissues, combined with patient clinicopathological and survival data for Cox regression analysis. The effect of knockdown SLC38A9 on the proliferation of pancreatic cancer cell lines was analyzed using the CCK8 assay, and the impact on migration and invasion was assessed using the Transwell chamber assay. Additionally, Western blot was employed to detect the effect of SLC38A9 knockdown on the expression of autophagy  associated proteins. Immunohistochemistry revealed that the positive expression rate of SLC38A9 in pancreaticcancer tissues was significantly higher than that in adjacent non-tumor tissues (38% vs 13%, P<0.001). Patients with high SLC38A9 expression had a median OS (overall survival) that was 25 months shorter than that of the control group (10 vs 35 months, P=0.013 6). Multivariate Cox analysis confirmed that high SLC38A9 expression was an independent risk factor for the prognosis of pancreatic cancer patients (HR=2.237, 95% CI: 1.210-4.136, P=0.010). Functional experiments showed that the CCK8 assay revealed a significant inhibition of pancreatic cancer cell proliferation upon SLC38A9 knockdown. The Transwell chamber assay results indicated that downregulating SLC38A9 significantly inhibited the migration and invasion of pancreatic cancer cells. Mechanistic studies found that knockdown of SLC38A9 led to downregulation of the autophagy key proteins LC3-II and Beclin-1, and accumulation of p62 (P<0.05), suggesting that SLC38A9 promotes tumor progression by activating autophagy. SLC38A9 is abnormally highly expressed in pancreatic cancer and serves as an independent adverse prognostic factor for patients. SLC38A9 may drive tumor malignancy via autophagy activation, highlighting its potential as a molecular marker for targeted therapy and prognosis in pancreatic cancer.

CSTR: 32200.14.cjcb.2025.12.0012