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Quantitative proteomic analysis of lung adenocarcinoma and squamous cell carcinoma primary tissues using high resolution mass spectrometry

ABSTRACT: Lung cancer is the leading cause of preventable death globally and is broadly classified into adenocarcinoma and squamous cell carcinoma depending upon cell type. In this study, we carried out mass spectrometry based quantitative proteomic analysis of lung adenocarcinoma and squamous cell carcinoma primary tissue by employing the isobaric tags for relative and absolute quantitation (iTRAQ) approach. Proteomic data was analyzed using SEQUEST search algorithm which resulted in identification of 25,998 peptides corresponding to 4,342 proteins of which 610 proteins were differentially expressed (≥ 2-fold) between adenocarcinoma and squamous cell carcinoma samples. These differentially expressed proteins were further classified by gene ontology for their localizations and biological processes. Pathway analysis of differentially expressed proteins revealed distinct alterations in networks and pathways in both adenocarcinoma and squamous cell carcinoma samples. In this study, we identified a subset of proteins that shows converse expression between lung adenocarcinoma and squamous cell carcinoma samples. Such proteins may serve as signature markers to distinguish between the two subtypes.

INSTRUMENT(S): Orbitrap Fusion ETD

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Lung

DISEASE(S): Lung Cancer

SUBMITTER: Aditi Chatterjee

LAB HEAD: Aditi Chatterjee

PROVIDER: PXD008700 | Pride | 2018-10-02

REPOSITORIES: Pride

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Data from quantitative proteomic analysis of lung adenocarcinoma and squamous cell carcinoma primary tissues using high resolution mass spectrometry.

Khan Aafaque Ahmad AA Mangalaparthi Kiran Kumar KK Advani Jayshree J Prasad T S Keshava TSK Gowda Harsha H Jain Deepali D Chatterjee Aditi A

Data in brief 20180622

Lung cancer is the leading cause of preventable death globally and is broadly classified into adenocarcinoma and squamous cell carcinoma. In this study, we carried out mass spectrometry based quantitative proteomic analysis of lung adenocarcinoma and squamous cell carcinoma primary tissue by employing the isobaric tags for relative and absolute quantitation (iTRAQ) approach. Proteomic data analyzed using SEQUEST algorithm resulted in identification of 25,998 peptides corresponding to 4342 protei ...[more]

PMID: 30229035

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Project description:Esophageal squamous cell carcinoma (ESCC) is one of the most common cancers with high mortality rate. Smoking is one of the established risk factors of ESCC. However, there is limited data on molecular alterations associated with cigarette smoke exposure in esophageal cells. Understanding the effects of cigarette smoke on esophageal squamous epithelial cells at a molecular level would lead to a better understanding of the pathobiology of ESCC which has implications for identification of early biomarkers and therapeutic targets. To investigate the effect of cigarette smoke exposure, we developed a cell line model where Het1A cells (non-neoplastic human esophageal epithelial cells) were chronically treated with cigarette smoke condensate (CSC) for 2 months, 4 months, 6 months and 8 months. We carried out comparative proteomic, phosphoproteomic and whole exome sequencing analyses on CSC treated and untreated cells. Increased cell proliferation and invasion of Het1A cells was observed after chronic exposure to cigarette smoke. Using quantitative proteomic and phosphoproteomic analyses, we identified 56 proteins and 296 phosphoproteins that showed differential expression. Bioinformatics analysis of differentially expressed proteins and phosphoproteins showed enrichment of molecules involved in DNA damage response pathway. Whole exome sequencing (WES) of CSC treated and untreated cells also revealed mutations and copy number alterations in genes associated with DNA damage response. By correlating WES, proteomic and phosphoproteomic results, we observed potential loss of function in HMGN2 and MED1 that were reported as potential tumor suppressors and are known to play important role in DNA damage response. We also observed decreased expression of HMGN2 in tissue section of ESCC. Overexpression of HMGN2 and MED1 lead to decreased proliferative and invasive ability of CSC treated cells. These findings suggest that cigarette smoke affects genes and proteins associated with DNA damage response pathways which might play a vital role in development of ESCC.

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