Fangyu Wang, Pengfei Lyu, Weimin Chen, Huiquan Gu, Wenlong Han, Yaolong Yu, Chen Chen, Rui He, Qiang Liu
FK506-binding protein 4 (FKBP4), also known as FKBP52, is an HSP90 co-chaperone associated with poor outcomes in lung adenocarcinoma (LUAD). We evaluated FKBP4 using TCGA-LUAD, cBioPortal, CellMiner, and H1299 cell data. Among 535 primary tumors, the 20 displayed FKBP4 correlations from each of the HALLMARK_APOPTOSIS and HALLMARK_PEROXISOME sets remained significant after set-wise Bonferroni correction. cBioPortal identified two FKBP4 coding alterations among 511 tumors (0.39%), without a recurrent hotspot. No CellMiner association remained significant after Benjamini-Hochberg correction across 263 activity profiles. Three siRNAs reduced FKBP4 transcript abundance in an archived qPCR screen, although independent transfections could not be confirmed. Only si-FKBP4-3 was assessed by CCK-8, and FKBP4 protein depletion was not confirmed during the assay window. In one archived experiment, mean OD450 values were higher at 48 and 72 h across five technical wells. Because CCK-8 reflects WST-8 reduction, this observation does not establish proliferation, survival, or another defined phenotype. The study therefore identifies tumor-level co-expression associations and a preliminary cellular observation requiring independent and orthogonal validation.