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Cranberry Proanthocyanidins Induce Apoptosis and Inhibit Acid-Induced Proliferation of Human Esophageal Adenocarcinoma Cells

Laura A. Kresty*, Amy B. Howell and Maureen Baird

Division of Hematology and Oncology, Department of Internal Medicine, College of Medicine, and Comprehensive Cancer Center, The Ohio State University, Columbus, Ohio 43210; and Blueberry and Cranberry Research Center, Rutgers University, Chatsworth, New Jersey 08019

J. Agric. Food Chem., 2008, 56 (3), pp 676–680

DOI: 10.1021/jf071997t

Publication Date (Web): January 23, 2008

* Address correspondence to this author at the Division of Hematology and Oncology, Department of Internal Medicine, CCC Building 302B, The Ohio State University, 410 W. 12th Ave., Columbus, OH 43210 [telephone (614) 688-7787 ; e-mail kresty.1@osu.edu].

Abstract

The occurrence of esophageal adenocarcinoma and its only recognized precursor lesion, Barrett’s esophagus, has rapidly increased during the past three decades. The precise reason for the rise remains to be elucidated, but increasing rates have been linked to multiple nutritional factors. Plant-based diets have generally been associated with a reduction of risk for esophageal adenocarcinoma and those of animal origin with risk escalation. Moreover, a number of recent in vitro and limited in vivo investigations have reported that cranberry extracts affect multiple cancer-associated processes in breast, colon, prostate, and other cancer cell lines of epithelial origin. Thus, this study sought to investigate the chemopreventive potential of a cranberry proanthocyanidin rich extract (PAC) in SEG-1 human esophageal adenocarcinoma (EAC) cells. PAC pretreatment significantly inhibited the viability and proliferation of EAC cells in a time- and dose-dependent manner. Moreover, PAC (50 µg/mL) significantly inhibited acid-induced cell proliferation of SEG-1 cells. PAC treatment induced cell cycle arrest at the G1 checkpoint and significantly reduced the percentage of SEG-1 cells in S-phase following 24 and 48 h of exposure. PAC treatment also resulted in significant induction of apoptosis. Thus, PAC modulates cell cycle regulation, aberrant proliferation, and apoptosis, all key biological processes altered during progression to esophageal adenocarcinoma. These findings support that further mechanistic studies are warranted to more fully elucidate the inhibitory potential of PAC against esophageal cancer.

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