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©2006 Baishideng Publishing Group Co., Limited. All rights reserved.
World J Gastroenterol. Dec 14, 2006; 12(46): 7428-7432
Published online Dec 14, 2006. doi: 10.3748/wjg.v12.i46.7428
Published online Dec 14, 2006. doi: 10.3748/wjg.v12.i46.7428
Nicotine as a mitogenic stimulus for pancreatic acinar cell proliferation
Parimal Chowdhury, Departments of Physiology and Biophysics, University of Arkansas for Medical Sciences, 4301 W Markham Street, Little Rock, Arkansas 72205, United States
Kodetthoor B Udupa, Departments of Physiology and Biophysics and Geriatrics, University of Arkansas for Medical Sciences, 4301 W Markham Street, Little Rock, Arkansas 72205, United States
Kodetthoor B Udupa, Medical Service, Central Arkansas Veterans Healthcare System, Little Rick, Arkansas 72205, United States
Author contributions: All authors contributed equally to the work.
Correspondence to: Parimal Chowdhury, PhD, University of Arkansas for Medical Sciences, 4301 W Markham Street, Little Rock, Arkansas 72205, United States. pchowdhury@uams.edu
Telephone: +1-501-6865443 Fax: +1-501-6868167
Received: July 29, 2006
Revised: August 5, 2006
Accepted: August 11, 2006
Published online: December 14, 2006
Revised: August 5, 2006
Accepted: August 11, 2006
Published online: December 14, 2006
Abstract
Cell proliferation is an important process in life for growth of normal and cancer cells. The signal transduction pathways activated during this process are strictly regulated. This editorial focuses on the role of nicotine, a mitogen, in the induction of signaling pathways resulting in proliferation of pancreatic tumor cells and compares these events with those in normal acinar cells isolated from the rat pancreas. The data shows striking similarities between these two cellular systems. In addition, the editorial reviews very recent literature of the contribution of MAPK signaling in cell lines associated with human diseases. A prospective cellular model of nicotine induced activation of MAPK cascade is presented.