SLIT2 inhibits lung adenocarcinoma progression by suppressing epithelial-mesenchymal transition.

Lung adenocarcinoma (LUAD), the most common subtype of lung cancer, is a major contributor to worldwide cancer deaths. Although the slit guidance ligand (SLIT) protein family is implicated in both normal biological processes and disease states, the specific role of SLIT2 in LUAD development remains unclear. To address this gap, the present study integrated bioinformatics analyses and experimental studies to investigate the functional significance and clinical relevance of SLIT2 in LUAD. The present analysis revealed that SLIT2 expression is significantly reduced in LUAD tissues and cell lines, and this decrease is associated with poorer patient outcomes. Functional experiments showed that inhibiting SLIT2 expression enhances LUAD cell growth, migration, invasion and epithelial-mesenchymal transformation of LUAD cells, whereas overexpression of SLIT2 can reverse these carcinogenic effects. Furthermore, it was observed that SLIT2 expression levels correlate with distinct patterns of immune cell infiltration in the tumor environment. These results suggested that targeting SLIT2 pathways could represent a novel therapeutic strategy for LUAD and further research is needed to explore the specific mechanisms through which SLIT2 exerts its tumor-suppressive effects and modulates immune responses. The current study enhances the understanding of LUAD biology and underscores the potential of SLIT2 as a biomarker and therapeutic target in LUAD.