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Ellagic acid inhibits proliferation and induces apoptosis in human glioblastoma cells
Wang, Dongliang; Chen, Qianxue; Liu, Baohui; Li, Yuntao; Tan, Yingqiu; Yang, Bangkun.
  • Wang, Dongliang; Wuhan University. Department of Neurosurgery. Hubei Province. CN
  • Chen, Qianxue; Wuhan University. Department of Neurosurgery. Hubei Province. CN
  • Liu, Baohui; Wuhan University. Department of Neurosurgery. Hubei Province. CN
  • Li, Yuntao; Wuhan University. Department of Neurosurgery. Hubei Province. CN
  • Tan, Yingqiu; Wuhan University. Department of Neurosurgery. Hubei Province. CN
  • Yang, Bangkun; Wuhan University. Department of Neurosurgery. Hubei Province. CN
Acta cir. bras ; 31(2): 143-149, Feb. 2016. graf
Article in English | LILACS | ID: lil-775565
ABSTRACT

PURPOSE:

To investigate the anticancer activity of ellagic acid (EA) in U251 human glioblastoma cells and its possible molecular mechanism.

METHODS:

The cells were treated with EA at various concentrations for different time periods. Cell viability and cell proliferation were detected by cell counting kit-8(CCK-8) assay and live/dead assay respectively. Cell apoptosis were measured with Annexin V-FITC/PI double staining method by flow cytometry and Mitochondrial membrane potential assay separately. Cell cycle was measured with PI staining method by flow cytometry. The expressions of Bcl-2, Survivin, XIAP, Caspase-3, Bax, JNK, p-JNK, ERK1/2, p-ERK1/2, p38, p-p38, DR4, DR5, CHOP and GRP78-related proteins were detected by western blot after EA treatment.

RESULTS:

Cell viability and proliferation of glioblastoma cells treated with EA were significantly lower than the control group. EA caused robust apoptosis of the glioblastoma cells compared to the control group. EA significantly decreased the proportion at G0/G1 phases of cell cycling accompanied by increased populations at S phase in U251 cell lines. And the expressions of anti-apoptotic proteins were dramatically down-regulated.

CONCLUSION:

Ellagic acid potentially up-regulated DR4, DR5 and MAP kinases (JNK, ERK1/2 and p38). EA also caused significant increase in the expressions of CHOP and GRP78. Our findings suggest that EA would be beneficial for the treatment of glioblastoma.
Subject(s)


Full text: Available Index: LILACS (Americas) Main subject: Apoptosis / Glioblastoma / Cell Proliferation / Ellagic Acid Limits: Humans Language: English Journal: Acta cir. bras Journal subject: General Surgery / Procedimentos Cir£rgicos Operat¢rios Year: 2016 Type: Article Affiliation country: China Institution/Affiliation country: Wuhan University/CN

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Full text: Available Index: LILACS (Americas) Main subject: Apoptosis / Glioblastoma / Cell Proliferation / Ellagic Acid Limits: Humans Language: English Journal: Acta cir. bras Journal subject: General Surgery / Procedimentos Cir£rgicos Operat¢rios Year: 2016 Type: Article Affiliation country: China Institution/Affiliation country: Wuhan University/CN