JPOST Repositoryapplication/xmlhttps://storage.jpostdb.org/JPST004583/files/cell_shHSP60_1_SWATH30.wiff.scanhttps://storage.jpostdb.org/JPST004583/files/cell_shcontrol2_SWATH3.wiff.scanhttps://storage.jpostdb.org/JPST004583/files/cell_shHSP60_2_IDA3.wiff.scanhttps://storage.jpostdb.org/JPST004583/files/cell_shcontrol2_IDA30.wiff.scanhttps://storage.jpostdb.org/JPST004583/files/cell_shcontrol1_IDA30.wiff.scanhttps://storage.jpostdb.org/JPST004583/files/cell_shHSP60_2_IDA30.wiff.scanhttps://storage.jpostdb.org/JPST004583/files/cell_shHSP60_1_IDA30.wiff.scanhttps://storage.jpostdb.org/JPST004583/files/cell_shcontrol2_IDA3.wiff.scanhttps://storage.jpostdb.org/JPST004583/files/cell_shHSP60_2_SWATH3.wiff.scanhttps://storage.jpostdb.org/JPST004583/files/cell_shHSP60_2_SWATH30.wiff.scanhttps://storage.jpostdb.org/JPST004583/files/cell_shcontrol3_SWATH30.wiff.scanhttps://storage.jpostdb.org/JPST004583/files/cell_shcontrol1_SWATH3.wiff.scanhttps://storage.jpostdb.org/JPST004583/files/cell_shHSP60_1_SWATH3.wiff.scanhttps://storage.jpostdb.org/JPST004583/files/cell_shHSP60_1_IDA3.wiff.scanhttps://storage.jpostdb.org/JPST004583/files/cell_shcontrol3_SWATH3.wiff.scanhttps://storage.jpostdb.org/JPST004583/files/cell_shcontrol1_SWATH30.wiff.scanhttps://storage.jpostdb.org/JPST004583/files/cell_shcontrol3_IDA3.wiff.scanhttps://storage.jpostdb.org/JPST004583/files/cell_shcontrol1_IDA3.wiff.scanhttps://storage.jpostdb.org/JPST004583/files/cell_shcontrol3_IDA30.wiff.scanhttps://storage.jpostdb.org/JPST004583/files/cell_shcontrol2_SWATH30.wiff.scanprimaryOK200ProteomicsSiripat AluksanasuwanHomo Sapiens (human)https://repository.jpostdb.org/entry/JPST004583Mahidol UniversityjPOSTfalseHeat shock protein family D member 1 (HSPD1) sustains ribosome biogenesis and protein synthesis as a component of its oncogenic function in lung adenocarcinomaLung adenocarcinoma (LUAD) is the most prevalent histological subtype of lung cancer. Heat shock protein family D member 1 (HSPD1 or HSP60), a multifunctional chaperone, has been implicated in promoting lung cancer progression by regulating tumor cell growth, cancer-associated fibroblast activation, and angiogenesis. Despite these roles, the molecular mechanisms underlying its oncogenic activity remain incompletely understood. In this study, we conducted a proteomic analysis and functional investigations on HSPD1-knockdown and control A549 cells. Knockdown of HSPD1 suppressed cell proliferation, disrupted cell-cycle progression, and had no significant effect on apoptosis. Additionally, HSPD1-knockdown cells exhibited reduced colony formation, migration, and invasion capabilities. SWATH-targeted proteomics revealed 21 significantly altered proteins, mainly involved in ribosome-related functions and associated with overall survival in LUAD patients. Reduced levels of ribosomal proteins and translational capacity were further confirmed by Western blot and protein synthesis assays. A decrease in ribosome abundance in HSPD1-knockdown cells was also observed under transmission electron microscopy. HSPD1 knockdown also sensitized cells to homoharringtonine, a ribosomal-targeting chemotherapeutic. Collectively, these findings indicate that HSPD1 acts as an oncogenic driver in LUAD by modulating ribosome-related pathways and protein synthesis.Tue Apr 28 00:00:00 GMT+01:00 2026PXD0776929606