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Background <p>SLC38A1 has been identified as a carcinogenic factor in the progression of colorectal, gastric, pancreatic, and other cancers. However, its involvement in lung adenocarcinoma (LUAD) remains unexplored in the literature.</p> Methods <p>The expression levels, diagnostic relevance, and clinical significance of SLC38A1 in LUAD were evaluated using data from the TCGA, XENA, and LCE databases, along with validation in samples from 10 LUAD patients at our hospital. Prognostic nomograms and risk models based on SLC38A1 were constructed. The functional roles and mechanisms of SLC38A1 in LUAD were investigated through CCK-8 assays, migration and invasion assays, Western blotting, GO and KEGG pathway analyses, and correlation analysis to explore its relationship with the immune microenvironment.</p> Results <p>SLC38A1 was overexpressed in both unpaired and paired LUAD samples, with a marked increase in early-stage LUAD. Overexpression of SLC38A1 correlated with diagnostic accuracy and poor overall survival (HR = 1.53; 95% CI = 1.15–2.04), disease-free survival (HR = 1.59; 95% CI = 1.1–2.3), and progression-free interval (HR = 1.51; 95% CI = 1.16–1.97). COX regression analysis identified SLC38A1 overexpression as an independent risk factor for poor prognosis in LUAD patients. High-risk scores and nomograms associated with SLC38A1 were significantly linked to adverse clinical outcomes. Genes co-expressed with SLC38A1 were involved in nuclear division, DNA replication, and the cell cycle. Silencing of SLC38A1 expression inhibited LUAD cell growth and migration. Furthermore, SLC38A1 overexpression was associated with immune cell infiltration in LUAD, including Th2 cells, Tcm, T helper cells, and immune markers such as CD8A, CD8B, and CTLA4.</p> Conclusion <p>SLC38A1 is upregulated in LUAD, and its overexpression is associated with poor prognosis, diagnostic accuracy, and immune cell infiltration. SLC38A1-based risk models and nomograms offer potential predictive tools for assessing prognosis in LUAD patients.</p>

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Elevated levels of SLC38A1 are correlated with an unfavorable prognosis, as well as accelerated cell proliferation and metastasis in lung adenocarcinoma

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年1月6日

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  • Tian Xia,
  • Qun-Xian Zhang,
  • Chang Liu,
  • Ming-Liang Wang,
  • Peng Miao,
  • Dan Li,
  • Li Wei

摘要

Background

SLC38A1 has been identified as a carcinogenic factor in the progression of colorectal, gastric, pancreatic, and other cancers. However, its involvement in lung adenocarcinoma (LUAD) remains unexplored in the literature.

Methods

The expression levels, diagnostic relevance, and clinical significance of SLC38A1 in LUAD were evaluated using data from the TCGA, XENA, and LCE databases, along with validation in samples from 10 LUAD patients at our hospital. Prognostic nomograms and risk models based on SLC38A1 were constructed. The functional roles and mechanisms of SLC38A1 in LUAD were investigated through CCK-8 assays, migration and invasion assays, Western blotting, GO and KEGG pathway analyses, and correlation analysis to explore its relationship with the immune microenvironment.

Results

SLC38A1 was overexpressed in both unpaired and paired LUAD samples, with a marked increase in early-stage LUAD. Overexpression of SLC38A1 correlated with diagnostic accuracy and poor overall survival (HR = 1.53; 95% CI = 1.15–2.04), disease-free survival (HR = 1.59; 95% CI = 1.1–2.3), and progression-free interval (HR = 1.51; 95% CI = 1.16–1.97). COX regression analysis identified SLC38A1 overexpression as an independent risk factor for poor prognosis in LUAD patients. High-risk scores and nomograms associated with SLC38A1 were significantly linked to adverse clinical outcomes. Genes co-expressed with SLC38A1 were involved in nuclear division, DNA replication, and the cell cycle. Silencing of SLC38A1 expression inhibited LUAD cell growth and migration. Furthermore, SLC38A1 overexpression was associated with immune cell infiltration in LUAD, including Th2 cells, Tcm, T helper cells, and immune markers such as CD8A, CD8B, and CTLA4.

Conclusion

SLC38A1 is upregulated in LUAD, and its overexpression is associated with poor prognosis, diagnostic accuracy, and immune cell infiltration. SLC38A1-based risk models and nomograms offer potential predictive tools for assessing prognosis in LUAD patients.