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. 2011 Dec 12;3(3):e36.
doi: 10.4081/dr.2011.e36. eCollection 2011 Oct 5.

Ellagic acid inhibits melanoma growth in vitro

J Daniel Jensen  1 , Jeffrey H Dunn  1 , Yuchun Luo  1 , Weimin Liu  1 , Mayumi Fujita  2 , Robert P Dellavalle  2
Affiliations

Ellagic acid inhibits melanoma growth in vitro

J Daniel Jensen et al. Dermatol Reports. .

Abstract

Ellagic is a polyphenolic compound with anti-fibrotic and antioxidant properties, and exhibits antitumor properties against various cancer cells in vitro. There are few studies, however, which examine the effects of ellagic acid on melanoma. In the present study, we observe effects of ellagic acid on melanoma cells in vitro. Three metastatic melanoma cell lines (1205Lu, WM852c and A375) were examined to determine the effects of ellagic acid on melanoma cell viability, cell-cycle, apoptosis, NF-κβ activity, and IL-1β & IL-8 secretion. Cell viability assays demonstrated that ellagic acid possesses an inhibitory effect on cell proliferation at concentrations between 25 and 100 µM. In addition, ellagic acid promoted G1 cell cycle arrest, increased levels of apoptosis and decreased synthesis of IL-1β and IL-8 in melanoma cells. Ellagic acid also decreased NF-κβ activity, suggesting at least one potential mechanism by which ellagic acid may exert its effects in melanoma cells. Our findings support further investigation into prospective roles for ellagic acid as a therapeutic, adjuvant, or preventive agent for melanoma.

Keywords: IL-1β; IL-8.; NF-κB; ellagic acid; melanoma.

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Figures

Figure 1
Figure 1
Cell growth over time with different concentrations of EA. A) WM852c and B) 1205Lu cells were incubated with different concentrations of EA for 24, 48, and 72 h and cell viability was measured using MTS assay.
Figure 2
Figure 2
A) Apoptotic cells at 72 h. Three cell lines (1205Lu, WM852c, A375) were incubated in 25, 50 and 100 µM concentrations of EA for 72 h. After staining for the apoptotic marker Annexin V, cell lines were then sorted with flow cytometry. B) Cell cycle analysis. WM852c cells were incubated for 48 h in 50 µM EA. After staining, cells were sorted according to the phase of their cell cycle.
Figure 3
Figure 3
Expression of NF-κβ after EA treatment. A plasmid containing a luciferase reporter gene under the control of NF-κβ was transfected into WM852c (A) and 1205LU cells (B) and measured after 24 hours incubation.
Figure 4
Figure 4
Expression of IL-1β and IL-8 cytokines after EA treatment. Metastatic melanoma cells were seeded and incubated for 24 h. Cells were then treated with 0 or 50 µM EA for 48 h. RNA was extracted from treated and untreated cells and measured by qRT-PCR. GAPDH was used as a control. *P <0.05
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