Ácido gálico é um agente seletivo que induz apoptose em células do câncer pancreático,
CFPAC-1 e MiaPaCa-2. Ocorre inibição da proliferação de modo tempo e dose dependente,
ativação das caspases-3 e 9, aumento das ERTOs, elevação da Bax e redução do potencial de
membrana mitocondrial. As células normais são poupadas
Gallic acid as a cancer-selective agent induces apoptosis in
pancreatic cancer cells.
Liu Z1, Li D, Yu L, Niu F.
Chemotherapy. 2012;58(3):185-94. doi: 10.1159/000337103. Epub 2012 Jun 22.
Author information
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1
School of Public Health, Jilin University, Changchun, PR China.
Abstract
BACKGROUND:
Gallic acid (GA) is a plant phenol isolated from water caltrop which is reported to have antiinflammatory and anti-cancer effects. In this study, the antiproliferative effect of GA on human
pancreatic cancer cell lines CFPAC-1 and MiaPaCa-2 as well as hepatocytes HL-7702 as
normal cells was examined. Particularly, the mechanism of GA-induced apoptosis in MiaPaCa-2
cells in vitro was further studied.
METHODS:
Cell viability was measured using SRB assay, and apoptosis was detected by Hoechst staining
and annexin V-PI staining assays. Mitochondrial membrane potential was detected by
rhodamine-123 staining. Flow cytometry analysis was employed to detect the apoptosis-related
events.
RESULTS:
GA inhibited the proliferation of CFPAC-1 and MiaPaCa-2 cells in a time- and dose-dependent
manner, with IC(50)S of 102.3 ± 2.4 and 135.2 ± 0.6 µM at 48 h, respectively. GA treatment led
to the increased proportion of cell apoptosis from 12.5 ± 0.72 to 78.3 ± 2.48% at the
concentrations of 6.25 and 25.0 µg/ml, which was evidenced again by chromatins staining
assay. Also, GA activated caspase-3, caspase-9, and reactive oxygen species, elevated Bax
expression and [Ca(2+)](i) and reduced mitochondrial membrane potential (ΔΨm) in MiaPaCa-2
cells. Remarkably, when compared with human normal cells HL-7702 (IC(50) >100 µg/ml), GA
showed selective toxicity for cancer cells.
CONCLUSIONS:
GA can function as a cancer-selective agent by inducing apoptosis in MiaPaCa-2 cells via the
mitochondria-mediated pathways. To the best of our knowledge, GA should open up new
opportunities for the therapy of pancreatic cancer.
Copyright © 2012 S. Karger AG, Basel.
PMID:
22739044