p53 proteins accumulated by heat stress associate with heat shock proteins HSP72/HSC73 in human glioblastoma cell lines

Matsumoto, Hideki; Shimura, Mari; Omatsu, Tokunori; Okaichi, Kumio; Majima, Hideyuki J.; Ohnishi, Takeo

doi:10.1016/0304-3835(94)90407-3

Cited by 86 publications

(34 citation statements)

References 19 publications

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“…T98G and AG0 have a mutated p53 (mp53) gene 29 and a wild-type p53 (wtp53) gene, 15 respectively. T98G cells were maintained in RPMI-1640 medium supplemented with 10% (v/v) fetal calf serum (FCS) and 0.01% sodium pyruvate, 2 mM L-glutamine, 100 U/ml penicillin and 100 g/ml streptomycin.…”

Section: Cell Cultures and Treatmentsmentioning

confidence: 99%

Bystander signaling between glioma cells and fibroblasts targeted with counted particles

Shao

Folkard

Michael

et al. 2005

Intl Journal of Cancer

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Radiation-induced bystander effects may play an important role in cancer risks associated with environmental, occupational and medical exposures and they may also present a therapeutic opportunity to modulate the efficacy of radiotherapy. However, the mechanisms underpinning these responses between tumor and normal cells are poorly understood. Using a microbeam, we investigated interactions between T98G malignant glioma cells and AG01522 normal fibroblasts by targeting cells through their nuclei in one population, then detecting cellular responses in the other co-cultured non-irradiated population. It was found that when a fraction of cells was individually irradiated with exactly 1 or 5 helium particles ( 3 He 2þ ), the yield of micronuclei (MN) in the non-irradiated population was significantly increased. This increase was not related to the fraction of cells targeted or the number of particles delivered to those cells. Even when one cell was targeted with a single 3 He 2þ , the induction of MN in the bystander non-irradiated population could be increased by 79% for AG01522 and 28% for T98G. Furthermore, studies showed that nitric oxide (NO) and reactive oxygen species (ROS) were involved in these bystander responses. Following nuclear irradiation in only 1% of cells, the NO level in the T98G population was increased by 31% and the ROS level in the AG0 population was increased by 18%. Treatment of cultures with 2-(4-carboxyphenyl)-4,4,5,5-tetramethyl-imidazoline-1-oxyl-3-oxide (c-PTIO), an NO scavenger, abolished the bystander MN induction in nonirradiated AG01522 cells but only partially in non-irradiated T98G cells, and this could be eliminated by treatment with either DMSO or antioxidants. Our findings indicate that differential mechanisms involving NO and ROS signaling factors play a role in bystander responses generated from targeted T98G glioma and AG0 fibroblasts, respectively. These bystander interactions suggest that a mechanistic control of the bystander effect could be of benefit to radiotherapy. ' 2005 Wiley-Liss, Inc.

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Section: Cell Cultures and Treatmentsmentioning

confidence: 99%

Bystander signaling between glioma cells and fibroblasts targeted with counted particles

Shao

Folkard

Michael

et al. 2005

Intl Journal of Cancer

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“…Human glioblastoma A-172 cells and U87MG (provided by JCRB, Setagaya, Tokyo, Japan) bearing the wtp53 gene (Matsumoto et al, 1994) are competent both in activating the expression of a p53-dependent reporter gene and WAF1 (Jung et al, 1995). T98G cells (provided by JCRB) bearing homologous mp53 have a single G to A transition in the third position of codon 237, resulting in a missense mutant of Met to Ile (Ullrich et al, 1992).…”

Section: Cell Culture and Reagentsmentioning

confidence: 99%

Poly(ADP-ribosyl)ation is required for p53-dependent signal transduction induced by radiation

et al. 1998

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p53 and poly(ADP-ribose) polymerase (PARP) are both DNA damage recognition proteins and can be functionally activated by DNA strand breaks. To understand the functional interaction between these two proteins, the eects of a PARP inhibitor, 3-aminobenzamide (3AB), on the p53 pathway were investigated in human glioblastoma cells with dierent p53 status. Consistent with previous studies, irradiation with g-rays induced both p53 and WAF1 accumulation in A-172 cells (wtp53) but not in T98G cells (mp53). However, the presence of 3AB but not its analog suppressed radiation-induced accumulation of wtp53 and the expression of WAF1 and MDM2. Similar results were also obtained from U87MG, another human glioblastoma cell line with wtp53 status. Northern blotting analysis showed that 3AB inhibited the g-ray-induced WAF1 gene expression. Moreover, 3AB but not its analog inhibited irradiationinduced activation of sequence-speci®c DNA binding of wtp53 as detected using 32 P-labeled or biotin-labeled p53 consensus sequence (p53CON). However, immunoblotting with an anti-poly(ADP-ribose) antibody showed that p53 proteins of the p53CON-bound fraction did not contain poly(ADP-ribose) (PAR). These ®ndings suggested that poly(ADP-ribosyl)ation is required for rapid accumulation of p53, activation of p53 sequence-speci®c DNA binding and its transcriptional activity after DNA damage.

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“…However, in addition to DNA-damaging agents, p53 has been shown to be activated by other cellular stresses such as hypoxia (Graeber et al, 1994), heat shock (Graeber et al, 1994;Matsumoto et al, 1994), cold shock (Ohnishi et al, 1998), media depletion (Zhan et al, 1993), microtuble-active drugs (Blagosklonny et al, 1995;Mukhopadhyay and Roth, 1997;Tishler et al, 1995), antioxidants (Liu et al, 1998;Plaumann et al, 1996), thymidine dinucleotides (Eller et al, 1997) or perturbations of nucleotide pools (Linke et al, 1996). It is thought that accumulation of p53 proteins as well as the activation of the sequence-speci®c DNA-binding activity of p53 are required to fully induce the p53 response (Hupp et al, 1992).…”

Section: Introductionmentioning

confidence: 99%

Inhibition of RNA polymerase II as a trigger for the p53 response

et al. 1999

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The mechanisms by which the p53 response is triggered following exposure to DNA-damaging agents have not yet been clearly elucidated. We and others have previously suggested that blockage of RNA polymerase II may be the trigger for induction of the p53 response following exposure to ultraviolet light. Here we report on the correlation between inhibition of mRNA synthesis and the induction of p53, p21 WAF1 and apoptosis in diploid human ®broblasts treated with either UV light, cisplatin or the RNA synthesis inhibitors actinomycin D, DRB, H7 and a-amanitin. Exposure to ionizing radiation or the proteasome inhibitor LLnL, however, induced p53 and p21 WAF1 without aecting mRNA synthesis. Importantly, induction of p53 by the RNA synthesis or proteasome inhibitors did not correlate with the induction of DNA strand breaks. Furthermore, cisplatin-induced accumulation of active p53 in repair-de®cient XP-A cells occurred despite the lack of DNA strand break induction. Our results suggest that the induction of the p53 response by certain toxic agents is not triggered by DNA strand breaks but rather, may be linked to inhibition of mRNA synthesis either directly by the poisoning of RNA polymerase II or indirectly by the induction of elongation-blocking DNA lesions.

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p53 proteins accumulated by heat stress associate with heat shock proteins HSP72/HSC73 in human glioblastoma cell lines

Cited by 86 publications

References 19 publications

Bystander signaling between glioma cells and fibroblasts targeted with counted particles

Bystander signaling between glioma cells and fibroblasts targeted with counted particles

Poly(ADP-ribosyl)ation is required for p53-dependent signal transduction induced by radiation

Inhibition of RNA polymerase II as a trigger for the p53 response

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