Effect of wild-type p53 gene transfection on the growth and radiotherapeutic sensitivity of human glioma cells

2005 ◽  
Vol 25 (4) ◽  
pp. 448-450
Author(s):  
Xiang Wei ◽  
Zhu Xianli ◽  
Zhao Hongyang
Keyword(s):  
Gene Transfection ◽  
Glioma Cells ◽  
P53 Gene ◽  
Human Glioma ◽  
Wild Type ◽  
Human Glioma Cells ◽  
Wild Type P53

Introduction of wild-type p53 enhances thrombospondin-1 expression in human glioma cells

2003 ◽  
Vol 191 (1) ◽  
pp. 109-119 ◽  
Author(s):  
Hironobu Harada ◽  
Kou Nakagawa ◽  
Masahiro Saito ◽  
Shohei Kohno ◽  
Shigeyuki Nagato ◽  
...  
Keyword(s):  
Glioma Cells ◽  
Human Glioma ◽  
Wild Type ◽  
Human Glioma Cells ◽  
Thrombospondin 1 ◽  
Wild Type P53

Wild-type p53—dependent etoposide-induced apoptosis mediated by caspase-3 activation in human glioma cells

2000 ◽  
Vol 93 (2) ◽  
pp. 289-297 ◽  
Author(s):  
Dali Yin ◽  
Norihiko Tamaki ◽  
Takashi Kokunai
Keyword(s):  
Glioma Cell ◽  
Glioma Cells ◽  
Human Glioma ◽  
Wild Type ◽  
Human Glioma Cells ◽  
Content Type ◽  
Low Concentrations ◽  
Wild Type P53 ◽  
Induced Apoptosis ◽  
Fine Print

Object. In an attempt to understand the roles of several apoptosis-related genes in human glioma cells, the authors investigated the relationship of wild-type p53, interleukin-1β—converting enzyme (ICE), caspase-3 (CPP32), bax, and bcl-2 to the apoptotic response of three glioma cell lines after treatment with etoposide.Methods. A human glioma cell line (U-87MG) that expresses wild-type p53, one that expresses mutant p53 (T-98G), and a T-98G derivative (T-98G/p53) that was transfected with a wild-type p53 expression vector (pCDM8-p53/neo) were used. Cell growth inhibition in response to etoposide was quantified using a modified methylthiazol tetrazolium colorimetric assay. Induction of apoptosis was evaluated using Hoechst 33258 staining and a DNA fragmentation assay. To study the expression of the apoptosis-related proteins and messenger RNAs in the three glioma cell lines, Western blotting and polymerase chain reaction were performed. A caspase assay and Western blot analysis were used to assess CPP32 and ICE protease activity. A CPP32 inhibition assay was used to determine whether a specific CPP32 inhibitor, DEVD-CHO, affects the apoptosis induced by etoposide in malignant glioma cells. Etoposide significantly inhibited the growth of U-87MG and T-98G/p53 cells in a dose-dependent manner compared with the growth of the T-98G cells. Treatment with low concentrations of etoposide resulted in the increased expression of wild-type p53; it also initiated CPP32 activity and induced apoptosis in the U-87MG cells. Apoptosis was not induced in T-98G cells at low concentrations of etoposide, although it was induced at high concentrations. Furthermore, low concentrations of etoposide also induced apoptosis in the T-98G/p53 cells by enhancing the expression of transfected wild-type p53, decreasing the expression of bcl-2, and activating CPP32 activity. However, etoposide did not alter the expression of bax and did not initiate ICE activity in these three glioma cell lines. Etoposide-induced apoptosis can be suppressed by the CPP32 inhibitor DEVD-CHO.Conclusions. These findings indicate that wild-type p53, CPP32, and bcl-2 may mediate apoptosis induced by etoposide. Forced expression of wild-type p53 increases etoposide cytotoxicity in human glioma cells by inducing apoptosis and may have important therapeutic implications.

Wild-type p53 gene transfection in human cultured sarcomas: Effect of CDDP

2001 ◽  
Author(s):  
Koji Endo ◽  
Itaru Kuratate ◽  
Mari Watanabe ◽  
Haruhiko Yoshida ◽  
Ryota Teshima ◽  
...  
Keyword(s):  
Gene Transfection ◽  
P53 Gene ◽  
Wild Type ◽  
Wild Type P53

Wild Type p53 Gene Sensitizes Rat C6 Glioma Cells to HSV-TK/ACV Treatment In Vitro and In Vivo

2010 ◽  
Vol 16 (4) ◽  
pp. 509-514 ◽  
Author(s):  
Qiang Huang ◽  
Zhibo Xia ◽  
Yongping You ◽  
Peiyu Pu
Keyword(s):  
Glioma Cells ◽  
P53 Gene ◽  
C6 Glioma ◽  
C6 Glioma Cells ◽  
Wild Type ◽  
Wild Type P53 ◽  
Rat C6 Glioma

scholarly journals Increased Radiosensitivity of p16 Gene-deleted Human Glioma Cells after Transfection with Wild-type p16 Gene

1997 ◽  
Vol 88 (1) ◽  
pp. 34-38 ◽  
Author(s):  
Junji Miyakoshi ◽  
Kaori Kitagawa ◽  
Nobuyuki Yamagishi ◽  
Shuji Ohtsu ◽  
Rufus S. Day ◽  
...  
Keyword(s):  
Glioma Cells ◽  
Human Glioma ◽  
Wild Type ◽  
Human Glioma Cells ◽  
P16 Gene

Effects of Gamma Knife surgery on C6 glioma in combination with adenoviral p53 in vitro and in vivo

2006 ◽  
Vol 105 (Supplement) ◽  
pp. 208-213 ◽  
Author(s):  
Desheng Xu ◽  
Qiang Jia ◽  
Yanhe Li ◽  
Chunsheng Kang ◽  
Peiyu Pu
Keyword(s):  
Glioma Cells ◽  
P53 Gene ◽  
Treated Group ◽  
C6 Glioma ◽  
C6 Glioma Cells ◽  
Survival Duration ◽  
Wild Type ◽  
Wild Type P53

ObjectThe authors sought to study the combined potential of wild-type p53 gene transfer and Gamma Knife surgery (GKS) for the treatment of glioblastomas multiforme. Modification of the radiation response in C6 glioma cells in vitro and in vivo by the wild-type p53 gene was investigated.MethodsStable expression of wild-type p53 in C6 cells was achieved by transduction of the cells with adenoviral p53. Two days later, some cells were treated with GKS. Forty-eight hours after irradiation, the comparative survival rate was assessed by monotetrazolium (MTT) assays. Treated and control C6 glioma cells (4 × 103 per well) were plated into a 96-well plate in octuplicate and tested every 24 hours. Meanwhile, immunohistopathological examination of proliferating cell nuclear antigen (PCNA) and terminal deoxynucleotidyl transferase—mediated deoxyuridine triphosphate (TUNEL) assays were performed. The MTT assays indicated the p53, GKS, and combined treated cells proliferated at a significantly lower rate than those of the control group (p < 0.01, Days 2–6) and the positive fraction of PCNA in p53-treated group and GKS-treated group was 70.18 ± 3.61 and 50.71 ± 2.61, respectively, whereas the percentage in the combined group was 30.68 ± 1.49 (p < 0.01).Fifty-six male Sprague–Dawley rats were anesthetized and inoculated with 106 cultured C6 glioma cells into the cerebrum. Forty-eight hours after transduction with adenoviral p53, some rats underwent GKS. A margin dose of 15 Gy was delivered to the 50% isodose line. Two days later, six rats in each group were killed. Their brains were removed and paraffin-embedded section were prepared for immunohistopathological examination and TUNEL assays. The remaining rats were observed for the duration of the survival period. The survival curve indicated that a modest but significant enhancement of survival duration was seen in the p53-treated or GKS alone groups, whereas a more marked and highly significant enhancement of survival duration was achieved when these two treatment modalities were combined. When PCNA expression was downregulated, apoptotic cells become obvious after TUNEL staining.Conclusions The findings of this study suggest that p53-based gene therapy in combination with GKS may be superior to single-modality treatment of C6 glioma.

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