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Resveratrol Inhibits Proliferation and Induces Apoptosis in Human Pancreatic Cancer Cells

Ding, Xian-Zhong; Adrian, Thomas E.

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Introduction Because of lack of early diagnosis and poor therapeutic responsiveness, median survival in patients with pancreatic cancer is <6 months, and survival beyond 5 years is rare. Thus, another dimension in chemotherapeutic agents for pancreatic cancer would be beneficial to control metastatic and unresectable disease. Resveratrol, a natural product from grapes, has been shown to be chemopreventive for carcinogen-induced skin cancer and also to inhibit proliferation of oral squamous, breast, colonic, and prostate cancer cells.

Aim To investigate the effect of resveratrol in pancreatic cancer.

Methodology To evaluate the potential role of resveratrol on pancreatic cancer cell proliferation, two human pancreatic cancer cell lines, PANC-1 and AsPC-1, were used.

Results Resveratrol inhibited proliferation of both PANC-1 and AsPC-1 in a concentration- and time-dependent manner as measured by [3H]thymidine incorporation. Cell number of both PANC-1 and AsPC-1 was also significantly decreased following 48 and 72 hours of treatment with 100 μmol/L resveratrol. The growth inhibition induced by resveratrol was accompanied by apoptotic morphologic changes, characterized by cell rounding and cell membrane blebbing suggesting apoptosis. Propidium iodide staining of DNA, measured by flow cytometry, showed a dramatic increase in the fraction of sub-G0/G1 cells following resveratrol treatment in both PANC-1 and AsPC-1. The substantial apoptosis inducted by resveratrol on these two cell lines was confirmed by the terminal deoxynucleotidyl transferase–mediated deoxyuridine triphosphate nick-end labeling assay.

Conclusion These findings suggest that the natural product resveratrol may have a potent antiproliferative effect on human pancreatic cancer with induction of apoptosis. Resveratrol is likely to be valuable for the management and prevention of human pancreatic cancer.

Department of Surgery, Northwestern University Medical School, Chicago, Illinois, U.S.A.

Manuscript received March 14, 2002;

revised manuscript accepted May 28, 2002.

Address correspondence and reprint requests to Dr. Thomas E. Adrian, Department of Surgery, Northwestern University Medical School, 303 East Chicago Avenue, Tarry Building 4–710, Chicago, IL 60611. E-mail: tadrian@northwestern.edu

© 2002 Lippincott Williams & Wilkins, Inc.