EFFECT OF EXOGENOUS WILD TYPE P53 ON MELANOMA CELL DEATH PATHWAYS INDUCED BY IRRADIATION AT DIFFERENT LET

2005 ◽  
Author(s):  
Feng-ling MIN ◽  
HONG ZHANG ◽  
Wen-jian LI ◽  
Qing-xiang Gao
Keyword(s):  
Cell Death ◽  
Melanoma Cell ◽  
Wild Type ◽  
Cell Death Pathways ◽  
Wild Type P53

EFFECT OF EXOGENOUS WILD-TYPE P53 ON MELANOMA CELL DEATH PATHWAYS INDUCED BY IRRADIATION AT DIFFERENT LINEAR ENERGY TRANSFER

2005 ◽  
Vol 41 (8) ◽  
pp. 284 ◽  
Author(s):  
FENG-LING MIN ◽  
HONG ZHANG ◽  
WEN-JIAN LI ◽  
QING-XIANG GAO ◽  
GUANG-MING ZHOU
Keyword(s):  
Cell Death ◽  
Energy Transfer ◽  
Melanoma Cell ◽  
Linear Energy Transfer ◽  
Wild Type ◽  
Cell Death Pathways ◽  
Wild Type P53

Cell cycle analysis of p53-induced cell death in murine erythroleukemia cells

1993 ◽  
Vol 13 (1) ◽  
pp. 711-719
Author(s):  
J J Ryan ◽  
R Danish ◽  
C A Gottlieb ◽  
M F Clarke
Keyword(s):  
Cell Death ◽  
G1 Arrest ◽  
Wild Type ◽  
Transfected Cells ◽  
Endogenous Expression ◽  
Erythroleukemia Cells ◽  
Wild Type P53 ◽  
G1 Cells ◽  
Murine Erythroleukemia ◽  
Murine Erythroleukemia Cells

A temperature-sensitive mutant of murine p53 (p53Val-135) was transfected by electroporation into murine erythroleukemia cells (DP16-1) lacking endogenous expression of p53. While the transfected cells grew normally in the presence of mutant p53 (37.5 degrees C), wild-type p53 (32.5 degrees C) was associated with a rapid loss of cell viability. Genomic DNA extracted at 32.5 degrees C was seen to be fragmented into a characteristic ladder consistent with cell death due to apoptosis. Following synchronization by density arrest, transfected cells released into G1 at 32.5 degrees C were found to lose viability more rapidly than did randomly growing cultures. Following release into G1, cells became irreversibly committed to cell death after 4 h at 32.5 degrees C. Commitment to cell death correlated with the first appearance of fragmented DNA. Synchronized cells allowed to pass out of G1 prior to being placed at 32.5 degrees C continued to cycle until subsequently arrested in G1; loss of viability occurred following G1 arrest. In contrast to cells in G1, cells cultured at 32.5 degrees C for prolonged periods during S phase and G2/M, and then returned to 37.5 degrees C, did not become committed to cell death. G1 arrest at 37.5 degrees C, utilizing either mimosine or isoleucine deprivation, does not lead to rapid cell death. Upon transfer to 32.5 degrees C, these G1 synchronized cell populations quickly lost viability. Cells that were kept density arrested at 32.5 degrees C (G0) lost viability at a much slower rate than did cells released into G1. Taken together, these results indicate that wild-type p53 induces cell death in murine erythroleukemia cells and that this effect occurs predominantly in the G1 phase of actively cycling cells.

scholarly journals Transcriptome analysis of xa5-mediated resistance to bacterial leaf streak in rice (Oryza sativa L.)

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Xiaofang Xie ◽  
Zhiwei Chen ◽  
Binghui Zhang ◽  
Huazhong Guan ◽  
Yan Zheng ◽  
...  
Keyword(s):  
Cell Death ◽  
Molecular Mechanism ◽  
Oryza Sativa L ◽  
Blast Resistance ◽  
Rna Seq ◽  
Bacterial Leaf Streak ◽  
Wild Type ◽  
Cell Death Pathways ◽  
Rnai Line ◽  
Transgenic Lines

Abstract Bacterial leaf steak (BLS) caused by Xanthomonas oryzae pv. oryzicola (Xoc) is a devastating disease in rice production. The resistance to BLS in rice is a quantitatively inherited trait, of which the molecular mechanism is still unclear. It has been proved that xa5, a recessive bacterial blast resistance gene, is the most possible candidate gene of the QTL qBlsr5a for BLS resistance. To study the molecular mechanism of xa5 function in BLS resistance, we created transgenic lines with RNAi of Xa5 (LOC_Os05g01710) and used RNA-seq to analyze the transcriptomes of a Xa5-RNAi line and the wild-type line at 9 h after inoculation with Xoc, with the mock inoculation as control. We found that Xa5-RNAi could (1) increase the resistance to BLS as expected from xa5; (2) alter (mainly up-regulate) the expression of hundreds of genes, most of which were related to disease resistance; and (3) greatly enhance the response of thousands of genes to Xoc infection, especially of the genes involved in cell death pathways. The results suggest that xa5 is the cause of BLS-resistance of QTL qBlsr5a and it displays BLS resistance effect probably mainly because of the enhanced response of the cell death-related genes to Xoc infection.

Adenovirus-mediated gene transfer of wild-type p53 results in melanoma cell apoptosisin vitro andin vivo

1995 ◽  
Vol 63 (5) ◽  
pp. 673-679 ◽  
Author(s):  
Corrado Cirielli ◽  
Teresa Riccioni ◽  
Chunlin Yang ◽  
Roberto Pili ◽  
Torsten Gloe ◽  
...  
Keyword(s):  
Gene Transfer ◽  
Melanoma Cell ◽  
Wild Type ◽  
Wild Type P53

Targeted Tumor Cell Death Induced by Autologous Tumor-Specific T Lymphocyte Recognition of Wild-Type p53-Derived Peptides

2005 ◽  
Vol 76 (2) ◽  
pp. 99-104
Author(s):  
Hideo Tsurushima ◽  
Yoshihiko Yoshii ◽  
Kam W Leong ◽  
Tadao Ohno
Keyword(s):  
Cell Death ◽  
Tumor Cell ◽  
T Lymphocyte ◽  
Autologous Tumor ◽  
Wild Type ◽  
Tumor Cell Death ◽  
Wild Type P53

scholarly journals The USP7 Inhibitor P5091 Induces Cell Death in Ovarian Cancers with Different P53 Status

2017 ◽  
Vol 43 (5) ◽  
pp. 1755-1766 ◽  
Author(s):  
Mengying Wang ◽  
Yayun Zhang ◽  
Taishu Wang ◽  
Jinrui Zhang ◽  
Zhu Zhou ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Ovarian Cancer ◽  
Cell Death ◽  
Cancer Cells ◽  
Pharmacological Intervention ◽  
Ovarian Cancer Cells ◽  
Mutant P53 ◽  
Wild Type ◽  
Ovarian Cancers ◽  
Wild Type P53

Background/Aims: Ovarian cancer is often diagnosed at later stages with poor prognosis. Recent studies have associated the expression of deubiquitylase USP7 with the survival of ovarian cancers. Being a cysteine protease, USP7 could become a target for pharmacological intervention. Therefore, in this study, we assessed the influence of its inhibitor P5091 on ovarian cancer cells. Methods: Ovarian cancer cells were treated with P5091, and cell proliferation was measured with MTT assay; cell morphology was inspected under a phase-contrast microscope; cell cycle and cell death were examined by flow cytometry. To gain mechanistic insights into its effects, immunoblotting was performed to detect USP7, HDM2, p53, p21, apoptosis and autophagy related proteins. Results: P5091 effectively suppressed the growth of ovarian cancer cells, caused cell cycle blockage, and induced necrosis and apoptosis with more severe phenotypes observed in HeyA8 cells with wild-type p53 than in OVCAR-8 cells with mutant p53. P5091 also prompted autophagy, with more efficient p62 degradation in HeyA8. Conclusion: P5091 shows efficacy in suppressing ovarian cancers harbouring wild-type and mutant p53. Its effects seemed to be enhanced by wild-type p53. The potency of this USP7 inhibitor also correlated with autophagy to some extent. Therefore, the pharmacological targeting of USP7 may serve as a potential therapeutic strategy and warrants further investigation.

scholarly journals Complementation by wild-type p53 of interleukin-6 effects on M1 cells: induction of cell cycle exit and cooperativity with c-myc suppression.

1993 ◽  
Vol 13 (12) ◽  
pp. 7942-7952 ◽  
Author(s):  
N Levy ◽  
E Yonish-Rouach ◽  
M Oren ◽  
A Kimchi
Keyword(s):  
Cell Cycle ◽  
Cell Death ◽  
Cell Cycle Arrest ◽  
Interleukin 6 ◽  
Quiescent State ◽  
Permissive Temperature ◽  
Wild Type ◽  
Antiproliferative Effects ◽  
Cycle Arrest ◽  
Wild Type P53

Stable transfection of M1 myeloid leukemia cells with a temperature-sensitive mutant of p53 results in two phenomena that are manifested exclusively at the permissive temperature. On one hand, activation of wild-type p53 by the temperature shift induced an apoptotic type of cell death which could be inhibited by interleukin-6 (IL-6) (E. Yonish-Rouach, D. Resnitzky, J. Lotem, L. Sachs, A. Kimchi, and M. Oren, Nature 352:345-347, 1991). On the other hand, as reported in this work, activated p53 complemented the antiproliferative effects of IL-6 in M1 cells. A shift to the permissive temperature concomitant with or early after IL-6 treatment imposed a novel pattern of cell cycle arrest in which about 95% of the cells were retained within a G0-like quiescent state. This phase was characterized by 2N DNA content and low RNA and protein content. On the molecular level, activation of wild-type p53 transrepressed the c-myc gene but not the cyclin A, D1, or D2 gene, which are all independently suppressed by IL-6 in M1 cells. To further analyze whether c-myc inhibition mediates or complements p53 effects, the p53-transfected M1 cells were infected with a retroviral vector expressing deregulated c-myc, refractory to p53 or IL-6 action. It was found that the process of cell death was not interrupted at all in these M1 c-myc-p53 double transfectants, suggesting that the transrepression of c-myc is not a major obligatory event mediating p53-induced cell death. In addition, some of the antiproliferative effects of activated p53, manifested in the presence of IL-6, could still be transmitted in the background of constitutive c-myc. Yet the context of deregulated c-myc interfered with the final accumulation of cells within a G0-like phase, suggesting complementary interactions between the outcome of p53 activation and of c-myc suppression in the control of cell cycle arrest.

scholarly journals Hematopoietic cells from mice deficient in wild-type p53 are more resistant to induction of apoptosis by some agents

Blood ◽  
1993 ◽  
Vol 82 (4) ◽  
pp. 1092-1096 ◽  
Author(s):  
J Lotem ◽  
L Sachs
Keyword(s):  
Cell Death ◽  
Tumor Development ◽  
Hematopoietic Cells ◽  
Suppressor Gene ◽  
Wild Type ◽  
Myeloid Progenitor Cells ◽  
Induction Of Apoptosis ◽  
Wild Type P53 ◽  
Macrophage Colony ◽  
Deficient Mice

Wild-type p53 is a tumor-suppressor gene that can induce cell death by apoptosis when expressed in myeloid leukemic and some other types of tumor cells. However, the question remained as to what extent wild-type p53 is a mediator of apoptosis in normal cells. We have used mice deficient in wild-type p53 to determine whether induction of apoptosis in hematopoietic cells from these p53 deficient mice is defective. We show here that bone marrow myeloid progenitor cells from p53-deficient mice are more resistant to induction of apoptosis when there was only a low concentration of the viability factors granulocyte-macrophage colony-stimulating factor; interleukins-1 alpha, -3, and -6; or stem cell factor; or when apoptosis was induced in these cells by irradiation or heat shock. The loss of one allele of wild-type p53 was sufficient for increased resistance. The higher resistance to apoptosis in p53-deficient mice was also found in irradiated thymocytes, but not in thymocytes treated with dexamethasone or in mature peritoneal granulocytes. The degree of resistance in irradiated myeloid progenitors and thymocytes showed a dosage effect of the number of wild- type p53 genes. The results show that wild-type p53 is involved in the induction of apoptosis by some agents in normal hematopoietic cells. Loss of wild-type p53 can, therefore, contribute to tumor development by decreasing cell death at low concentrations of viability factors and after exposure to a DNA-damaging agent. The results also show that there are wild-type p53-dependent and -independent pathways of normal cell apoptosis.

scholarly journals Molecular determinants of cell death induction following adenovirus-mediated gene transfer of wild-type p53 in prostate cancer cells

2000 ◽  
Vol 91 (2) ◽  
pp. 159-166
Author(s):  
Guido Schumacher ◽  
Elizabeth M. Bruckheimer ◽  
Alexander W. Beham ◽  
Tsuyoshi Honda ◽  
Shawn Brisbay ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cell Death ◽  
Gene Transfer ◽  
Cancer Cells ◽  
Wild Type ◽  
Prostate Cancer Cells ◽  
Molecular Determinants ◽  
Wild Type P53

scholarly journals Transcriptome Analysis of xa5-mediated Resistance to Bacterial Leaf Streak in Rice (Oryza sativa L.)

2019 ◽  
Author(s):  
Xiaofang Xie ◽  
Zhiwei Chen ◽  
Huazhong Guan ◽  
Yan Zheng ◽  
Jing Zhang ◽  
...  
Keyword(s):  
Cell Death ◽  
Molecular Mechanism ◽  
Oryza Sativa L ◽  
Blast Resistance ◽  
Rna Seq ◽  
Bacterial Leaf Streak ◽  
Wild Type ◽  
Cell Death Pathways ◽  
Rnai Line ◽  
Transgenic Lines

AbstractBacterial leaf steak (BLS) caused by Xanthomonas oryzae pv. oryzicola (Xoc) is a devastating disease in rice production. The resistance to BLS in rice is a quantitatively inherited trait, of which the molecular mechanism is still unclear. It has been proved that xa5, a recessive bacterial blast resistance gene, is the most possible candidate gene of the QTL qBlsr5a for BLS resistance. To study the molecular mechanism of xa5 function in BLS resistance, we created transgenic lines with RNAi of Xa5 (LOC_Os05g01710) and used RNA-seq to analyze the transcriptomes of a Xa5-RNAi line and the wild-type line at 9 h after inoculation with Xoc, with the mock inoculation with water as control. The results showed that Xa5-RNAi could (1) increase the resistance to BLS as expected from xa5; (2) alter (mainly up-regulate) the expression of hundreds of genes, most of which were related to disease resistance; and (3) greatly enhance the response of thousands of genes to Xoc infection, especially of the genes involved in cell death pathways, suggesting that xa5 displays BLS resistance effect probably mainly because of the enhanced response of the cell death-related genes to Xoc infection.

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