Lung cancer is the most common cancer and the primary cause of cancer-related deaths worldwide. Solute carrier family 39 member 5 (SLC39A5) regulates cellular zinc homeostasis and plays a vital role in several human cancers. However, the clinical significance and biological function of SLC39A5 in lung adenocarcinoma (LUAD) remain unclear. Hence, we sought to elucidate the role of SLC39A5 in LUAD pathophysiology in this study. The expression and clinical significance of SLC39A5 were evaluated using The Cancer Genome Atlas, the Gene Expression Omnibus, and tissue microarray data. We used the Cell Counting Kit-8, flow cytometry, western blotting, and quantitative reverse transcriptase-polymerase chain reaction analyses to determine the function of SLC39A5 in vitro. We also used a mouse xenograft model to evaluate the function of SLC39A5 in vivo. Our results indicate that SLC39A5 was upregulated in LUAD tissues compared with that in adjacent non-tumor lung tissues. SLC39A5 overexpression correlated with poor survival in patients with LUAD. SLC39A5 promoted LUAD cell proliferation by accelerating the G1-to-S phase transition and inhibiting apoptosis. SLC39A5 knockdown inhibited the tumorigenesis of LUAD cells in a nude mouse model of xenograft tumors. SLC39A5 promoted LUAD cell proliferation by activating the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (AKT) signaling. SLC39A5 played an oncogenic role in LUAD by activating the PI3K/AKT signaling. Hence, SLC39A5 may serve as a novel prognostic biomarker and potential therapeutic target for LUAD.
Keywords: Apoptosis; Lung adenocarcinoma; PI3K/AKT signaling; Proliferation; SLC39A5.
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