Cisplatin downregulates BCL2L12, a novel apoptosis-related gene, in glioblastoma cells
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  • 作者:Mahdieh Sadat Taghavi (1)
    Azim Akbarzadeh (2)
    Reza Mahdian (3)
    Kayhan Azadmanesh (4)
    Gholamreza Javadi (1)
  • 关键词:BCL2L12 ; Cisplatin ; Apoptosis ; Glioblastoma multiforme
  • 刊名:In Vitro Cellular & Developmental Biology - Animal
  • 出版年:2013
  • 出版时间:June 2013
  • 年:2013
  • 卷:49
  • 期:6
  • 页码:465-472
  • 全文大小:416KB
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  • 作者单位:Mahdieh Sadat Taghavi (1)
    Azim Akbarzadeh (2)
    Reza Mahdian (3)
    Kayhan Azadmanesh (4)
    Gholamreza Javadi (1)

    1. Department of Biology, Science and Research Branch, Islamic Azad University, Tehran, Iran
    2. Pilot Biotechnology Department, Pasteur Institute of Iran, Tehran, Iran
    3. Biotechnology Research Center, Molecular Medicine Department, Pasteur Institute of Iran, Tehran, Iran
    4. Virology Department, Pasteur Institute of Iran, Tehran, Iran
文摘
Glioblastoma progression is mainly characterized by intense apoptosis resistance and marked necrosis. Over-expression of BCL2L12, a novel member of Bcl-2 family has been shown in primary glioblastoma. BCL2L12 blocks effective caspase-3/7 maturation and inhibits p53 tumor suppressor, deriving resistance toward apoptosis and inducing extensive cell necrosis. Cisplatin is a major chemotherapeutic agent which has a broad range of anti-neoplastic activities including apoptosis induction. To investigate the effect of cisplatin on the expression of BCL2L12 in glioblastoma cells, two glioblastoma cell lines were treated with different concentrations of cisplatin for 48?h. The cell viability and IC50 was determined using MTT assay. Then, the two glioblastoma cell lines were treated with 48?h IC50 concentration of cisplatin for 24, 48, and 72?h. Apoptosis induction was analyzed by fluorescence microscopy and flow cytometry. Gene expression study was performed on BCL2L12 and TBP as target and internal control genes, respectively. The quantitative real-time polymerase chain reaction results showed that BCL2L12 gene expression was significantly (p--.001) downregulated in the presence of cisplatin. In conclusion, cisplatin treatment induced a time-dependent apoptosis in glioblastoma cells, at least partially via downregulation of BCL2L12 gene expression.

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