LINC00885 promotes lung squamous cell carcinoma by upregulating SLBP expression to activate PI3K/Akt pathway.

Lung squamous cell carcinoma (LUSC) remains an aggressive malignancy with limited therapeutic options and poor prognosis. Understanding the molecular drivers of LUSC pathogenesis is crucial for developing novel interventions. This study investigates the functional significance and mechanistic basis of long non-coding RNA LINC00885 in LUSC progression. We employed integrated methodologies including bioinformatic analysis, clinical specimen validation, in vitro functional assays (EdU incorporation, colony formation, Transwell migration/invasion), molecular profiling (qPCR, immunoblotting, northern blot, fluorescence in situ hybridization, subcellular fractionation), mechanistic investigations (chromatin isolation by RNA purification, luciferase reporter assays), and in vivo xenograft modeling. LINC00885 was significantly upregulated in LUSC clinical tissues and cell lines. Genetic depletion of LINC00885 suppressed malignant phenotypes including cellular proliferation, migration, invasion, and epithelial-mesenchymal transition. Mechanistically, LINC00885 directly bound and repressed tumor-suppressive miR-654-3p, which targeted stem-loop binding protein (SLBP). LINC00885 activated PI3K/Akt signaling through SLBP upregulation, and either SLBP overexpression or miR-654-3p depletion rescued the tumor-suppressive effects of LINC00885 knockdown. Xenograft models confirmed LINC00885 silencing significantly inhibited tumor growth in vivo. LINC00885 promotes LUSC progression via the miR-654-3p/SLBP/PI3K/Akt signaling axis.