Nicotine alters the proteome of two human pancreatic duct cell lines

Cigarette smoking is a known risk factor of pancreatic disease. Nicotine--a major cigarette tobacco component--can traffic through the circulatory system and may induce fibrosis and metastasis, hallmarks of chronic pancreatitis and pancreatic adenocarcinoma, respectively. However, at the biomolecular level, particularly in pancreatic research, the effects of nicotine remain unresolved.

The effects of nicotine on the proteomes of two pancreatic duct cell lines-an immortalized normal cell line (HPNE) and a cancer cell line (PanC1)- were investigated using mass spectrometry-based proteomics. For each cell line, the global proteomes of cells exposed to nicotine for 24 hrs were compared with untreated cells in triplicate using 6-plex tandem mass tag-based isobaric labeling techniques.

Over 5,000 proteins were detected per cell line. Of these, over 900 proteins were differentially abundant with statistical significance (corrected P-value <0.01) upon nicotine treatment, 57 of which were so in both cell lines. Amyloid precursor protein, previously observed to increase expression in pancreatic stellate cells when exposed to nicotine, was also up-regulated in both cell lines.In general, the two cell lines varied in the classes of proteins altered by nicotine treatment, supporting published evidence that nicotine may play different roles in the initiation and progression of pancreatic disease.

Understanding the underlying mechanisms associating nicotine with pancreatic function is paramount to intervention aiming to retard, arrest, or ameliorate pancreatic disease.