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Feasibility Evaluation of Emodin (Rhubarb Extract) as an Inhibitor of Pancreatic Cancer Cell Proliferation In Vitro
Author(s) -
Cai Jun,
Razzak Anthony,
Hering Justin,
Saed Abdul,
Babcock Tricia A.,
Helton Scott,
Espat N. Joseph
Publication year - 2008
Publication title -
journal of parenteral and enteral nutrition
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.935
H-Index - 98
eISSN - 1941-2444
pISSN - 0148-6071
DOI - 10.1177/0148607108314371
Subject(s) - emodin , pancreatic cancer , apoptosis , propidium iodide , cell growth , flow cytometry , cancer research , cell cycle , cell culture , microbiology and biotechnology , chemistry , biology , cancer , medicine , programmed cell death , biochemistry , genetics
Emodin is a commonly used traditional herbal treatment in China, including use for pancreatic malignancy. In this study, the potential for emodin to inhibit pancreatic cancer cell proliferation was examined using 4 human pancreatic adenocarcinoma cell lines: Mia Paca‐2, BxPC‐3, Panc‐1, and L3.6pl. WST‐1 proliferation, propidium iodide flow cytometry cell cycle analysis, and poly‐ADP‐ribose polymerase (PARP) Western blot analysis were performed. Forty‐eight‐hour treatment with 50 μM emodin inhibited proliferation in Mia Paca‐2 cells by 42%, BxPc‐3 by 38%, L3.6pl by 56%, and Panc‐1 by 18% (all P < .01). In three‐fourths of the cell lines, emodin treatment resulted in an increase (from 4.7% to 22%) in the cell population number in apoptosis when measured by flow cytometric analysis. Mia Paca‐2 revealed a significant PARP cleavage product when compared with control. These feasibility experiments provide initial evidence that emodin exerts an antiproliferative effect, likely through apoptosis induction‐related mechanism(s), that is reproducible in various human pancreatic cancer cell lines.