Dataset Information

Effect of cigarette smoke on microRNA expression in H292 lung cancer cells

ABSTRACT: Cigarette smoke has been associated with the development of various lung diseases including cancer. Dysregulation of miRNAs is known to affect protein expression which leads to diverse functional consequences. Investigating miRNA and protein expression in response to cigarette smoke exposure can lead to the identification of potential therapeutic and chemopreventive targets. We employed a SILAC-based quantitative proteomic analysis to identify proteins differentially expressed in response to cigarette smoke in H292 lung cancer cells. LC-MS/MS analysis led to the identification of 3,959 proteins, of which, 303 proteins were overexpressed and 112 proteins were found to be downregulated in cigarette smoke-treated H292 cells.

INSTRUMENT(S): LTQ Orbitrap Velos

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Epithelial Cell Of Lung

DISEASE(S): Non-small Cell Lung Carcinoma

SUBMITTER: Akhilesh Pandey

LAB HEAD: Akhilesh Pandey

PROVIDER: PXD003086 | Pride | 2018-10-25

REPOSITORIES: Pride

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Publications

Long-Term Cigarette Smoke Exposure and Changes in MiRNA Expression and Proteome in Non-Small-Cell Lung Cancer.

Advani Jayshree J Subbannayya Yashwanth Y Patel Krishna K Khan Aafaque Ahmad AA Patil Arun H AH Jain Ankit P AP Solanki Hitendra S HS Radhakrishnan Aneesha A Pinto Sneha M SM Sahasrabuddhe Nandini A NA Thomas Joji K JK Mathur Premendu P PP Nair Bipin G BG Chang Xiaofei X Prasad T S Keshava TSK Sidransky David D Gowda Harsha H Chatterjee Aditi A

Omics : a journal of integrative biology 20170701 7

Chronic exposure to cigarette smoke markedly increases the risk for lung cancer. Regulation of gene expression at the post-transcriptional level by miRNAs influences a variety of cancer-related interactomes. Yet, relatively little is known on the effects of long-term cigarette smoke exposure on miRNA expression and gene regulation. NCI-H292 (H292) is a cell line sensitive to cigarette smoke with mucoepidermoid characteristics in culture. We report, in this study, original observations on long-te ...[more]

PMID: 28692419

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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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	H292_SILAC_CSC_TP_01.raw	Raw
	H292_SILAC_CSC_TP_02.raw	Raw
	H292_SILAC_CSC_TP_03.raw	Raw
	H292_SILAC_CSC_TP_04.raw	Raw
	H292_SILAC_CSC_TP_05.raw	Raw