LINC00936 Suppresses Non-Small Cell Lung Cancer Progression Through Modulation of the Ras/MAPK Signaling Pathway

Objective: To characterize the tumor-suppressive role of LINC00936 in non-small cell lung cancer (NSCLC) through mechanistic exploration of its regulatory pathways. Methods: Bioinformatics interrogation of TCGA/NSCLC cohorts assessed LINC00936 expression, clinical correlations, and immune contexture. Functional enrichment analyses predicted pathway associations. In H1299 cells, LINC00936 overexpression (plasmid) and knockdown (siRNA) models were validated by RT-qPCR. Transcriptomic profiling identified differentially expressed genes (DEGs) subjected to KEGG pathway analysis. Results: LINC00936 was significantly downregulated in NSCLC tissues (TCGA, P < 0.05) and cell lines (vs. 16-HBE, P < 0.05), correlating with poor prognosis and altered tumor-infiltrating immune subsets. DEG enrichment implicated Ras/MAPK signaling as the dominant pathway (FDR < 0.05). Successful LINC00936 modulation (overexpression/knockdown, P < 0.05) confirmed its regulatory capacity. Conclusion: LINC00936 acts as a tumor suppressor in NSCLC via Ras/MAPK pathway modulation, proposing its therapeutic candidacy for precision oncology strategies.