Scientific paperLeptin stimulates esophageal adenocarcinoma growth by nonapoptotic mechanisms
Section snippets
Cell culture and reagents
Human esophageal adenocarcinoma cells (BIC-1 and SEG-1) were derived from Barrett's-associated adenocarcinomas of the distal esophagus [13] and generously provided as a gift by David G. Beer (University of Michigan, Ann Arbor, Michigan). Cells were maintained as monolayers in DMEM media with L-glutamine (Gibco Invitrogen, Carlsbad, California), supplemented with 10% FBS (Biowhittaker, Walkersville, Maryland) and streptomycin (100 μg/mL), and maintained in humidified air at 5% CO2 in a 37°C
The MTT assay
The MTT colorimetric assay was performed to detect tumor cell viability after incubation. The MTT, a tetrazolium dye (3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide; thiazolyl blue [Sigma, St. Louis, Missouri]) was added to the each well as described previously [14]. Plates were incubated in the presence of MTT dye for 4 hours. Mitochondrial dehydrogenase activity reduced the yellow MTT dye to a purple formazan, which was then solubilized with acidified isopropanol and absorbance
Effect of leptin on cell proliferation
The effects of leptin on esophageal adenocarcinoma tumor cell growth were assessed. Tumor cells were treated with vehicle or human recombinant leptin in concentrations ranging from 0, 40, and 80 ng/mL, and the effects on cell growth were determined after 24 hours of treatment. Exogenous leptin stimulated cell proliferation in both cell lines as shown in Table 1. Administration of leptin at the 40 ng/mL concentration showed no significant change in proliferation for either cell type after 24
Comments
Adenocarcinomas of the esophagus have gained considerable interest recently owing to a rapid increase in reported cases [10]. Devesa et al [11] evaluated incidence trends in the United States and noted a 350% increase in the incidence of esophageal adenocarcinoma between 1976 and 1994. Others have estimated an average annual increase in incidence of 20.6% for the United States, with even higher incidence rates noted for Great Britain, Australia, and the Netherlands [15]. One risk factor that
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2011, Cancer LettersCitation Excerpt :These findings could suggest that these factors may, at least in part, be driving the proliferation of tumour cells. Similar to other studies which have examined the impact of individual adipocytokines, such as leptin, on tumour cell proliferation [34,35], we observed a significant and dose dependent increase in both oesophageal and colorectal tumour cell proliferation in response to the two cytokines which were significantly higher in visceral adipose tissue, VEGF and IL-6. Neutralization experiments reveal the importance of VEGF in promoting tumour cell proliferation in both oesophageal and colorectal models.