pRb2/p130 promotes radiation-induced cell death in the glioblastoma cell line HJC12 by p73 upregulation and Bcl-2 downregulation

被引:17
作者
Pucci, B
Claudio, PP
Masciullo, V
Bellincampi, L
Terrinoni, A
Khalili, K
Melino, G
Giordano, A
机构
[1] Temple Univ, Sbarro Inst Canc Res & Mol Med, Coll Sci & Technol, Philadelphia, PA 19122 USA
[2] Jefferson Med Coll, Dept Pathol Anat & Cell Biol, Philadelphia, PA 19107 USA
[3] Univ Naples Federico II, Dipartimento Sci Odontostomatol & Maxillo Faccial, I-80131 Naples, Italy
[4] Univ Roma Tor Vergata, Dipartimento Med Interna, I-00133 Rome, Italy
[5] Univ Roma Tor Vergata, Biochim Lab, IDI, IRCCS,Dipartimento Med Sperimentale & Sci Biochim, I-00133 Rome, Italy
[6] Temple Univ, Ctr Neuro Virol & Canc Biol, Philadelphia, PA 19122 USA
关键词
apoptosis; gamma-radiation; pRb2/p130; glioblastoma; p73; Bcl-2; cell cycle;
D O I
10.1038/sj.onc.1205750
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
This study shows that in the glioblastoma hamster cell line HJC12 the retinoblastoma family member pRb2/p130 enhances gamma-radiation-induced cell death. In HJC12 cells the tetracycline-regulated expression of pRb2/p130 increased the percentage of gamma-radiation-induced apoptotic cells from 27 to 47%. pRb2/p130 overexpression was associated with the downregulation of the anti-apoptotic factor Bcl-2 and the upregulation of the steady-state protein levels of the pro-apoptotic transcription factor p73. In particular, RT-PCR showed a significant increase in the expression of the p73delta isoform when pRb2/p130 was overexpressed. The ability of pRb2/p130 to modulate apoptosis was not associated with its role in mediating G0/G1 arrest during cell cycle progression. Our data suggest a role for pRb2/p130 in glioblastoma gamma-radiation-induced cell death, indicating that the antitumoral action of pRb2/p130 can regulate both inhibition of cell cycle progression and induction of cell death.
引用
收藏
页码:5897 / 5905
页数:9
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