Phosphoproteomic analysis reveals cytoskeletal remodelling via CDC42-PAK signaling in lung mucoepidermoid cells upon chronic exposure to cigarette

ABSTRACT: Despite the fact that smoking is the major cause of lung cancer, there is no clear mechanism detailing how chronic exposure of cigarette smoke alters the global signaling in lung cells. To investigate the altered signaling in lung cells, in this study, we carried out SILAC-based quantitative phosphoproteomic analysis of H292 cells chronically exposed to cigarette smoke. Using high resolution Orbitrap Velos mass spectrometer, we identified hyperphosphorylation of 493 sites which corresponds to 341 proteins and 195 hypophosphorylated sites mapping to 142 proteins, upon smoke exposure (2.0-fold). Bioinformatics analysis revealed differentially phosphotylated proteins were involved in multiple cellular processes including cellular polarity, cytoskeletal remodelling, cellular migration, protein synthesis, autophagy and apoptosis. The present study will significantly improve the current knowledge of smoke mediated signaling in lung cells, which in turn may aid in the development of targeted therapies specially for smokers.

INSTRUMENT(S): LTQ Orbitrap Velos

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Lung

DISEASE(S): Non-small Cell Lung Carcinoma

SUBMITTER: Aditi Chatterjee  

LAB HEAD: Aditi Chatterjee

PROVIDER: PXD006672 | Pride | 2018-10-24

REPOSITORIES: Pride