scholarly journals Selective Induction of Necrotic Cell Death in Cancer Cells by β-Lapachone through Activation of DNA Damage Response Pathway

Cell Cycle ◽  
2006 ◽  
Vol 5 (17) ◽  
pp. 2029-2035 ◽  
Author(s):  
Xiangao Sun ◽  
Youzhi Li ◽  
Wei Li ◽  
Bin Zhang ◽  
A.J. Wang ◽  
...  
Keyword(s):  
Dna Damage ◽  
Cell Death ◽  
Cancer Cells ◽  
Dna Damage Response ◽  
Necrotic Cell Death ◽  
Necrotic Cell ◽  
Damage Response ◽  
Dna Damage Response Pathway

scholarly journals MacroH2A1 Regulation of Poly(ADP-Ribose) Synthesis and Stability Prevents Necrosis and Promotes DNA Repair

2019 ◽  
Vol 40 (1) ◽  
Author(s):  
Penelope D. Ruiz ◽  
Gregory A. Hamilton ◽  
Jong Woo Park ◽  
Matthew J. Gamble
Keyword(s):  
Dna Damage ◽  
Cell Death ◽  
Dna Damage Response ◽  
Oxidative Dna Damage ◽  
Necrotic Cell Death ◽  
Necrotic Cell ◽  
Damage Response ◽  
Parp Activity ◽  
Kinetics Of

ABSTRACT Through its ability to bind the ends of poly(ADP-ribose) (PAR) chains, the function of the histone variant macroH2A1.1, including its ability to regulate transcription, is coupled to PAR polymerases (PARPs). PARP1 also has a major role in DNA damage response (DDR) signaling, and our results show that macroH2A1 alters the kinetics of PAR accumulation following acute DNA damage by both suppressing PARP activity and simultaneously protecting PAR chains from degradation. In this way, we demonstrate that macroH2A1 prevents cellular NAD+ depletion, subsequently preventing necrotic cell death that would otherwise occur due to PARP overactivation. We also show that macroH2A1-dependent PAR stabilization promotes efficient repair of oxidative DNA damage. While the role of PAR in recruiting and regulating macrodomain-containing proteins has been established, our results demonstrate that, conversely, macrodomain-containing proteins, and specifically those containing macroH2A1, can regulate PARP1 function through a novel mechanism that promotes both survival and efficient repair during DNA damage response.

A shared DNA-damage-response pathway for induction of stem-cell death by UVB and by gamma irradiation

DNA Repair ◽  
2010 ◽  
Vol 9 (9) ◽  
pp. 940-948 ◽  
Author(s):  
T. Furukawa ◽  
M.J. Curtis ◽  
C.M. Tominey ◽  
Y.H. Duong ◽  
B.W.L. Wilcox ◽  
...  
Keyword(s):  
Dna Damage ◽  
Cell Death ◽  
Stem Cell ◽  
Gamma Irradiation ◽  
Dna Damage Response ◽  
Damage Response ◽  
Dna Damage Response Pathway

Cytotoxic mechanism of novel compound jiangxienone from Cordyceps jiangxiensis against cancer cells involving DNA damage response pathway

2014 ◽  
Vol 49 (4) ◽  
pp. 697-705 ◽  
Author(s):  
Yu-Hong Lü ◽  
Wei-Dong Pan ◽  
Jian-Hui Xiao ◽  
Zhong-Hua Sun ◽  
Jian-Jiang Zhong
Keyword(s):  
Dna Damage ◽  
Cancer Cells ◽  
Dna Damage Response ◽  
Damage Response ◽  
Cytotoxic Mechanism ◽  
Dna Damage Response Pathway

scholarly journals Mitochondrial glutamine metabolism regulates sensitivity of cancer cells after chemotherapy via amphiregulin

2021 ◽  
Vol 7 (1) ◽  
Author(s):  
Sunsook Hwang ◽  
Seungyeon Yang ◽  
Minjoong Kim ◽  
Youlim Hong ◽  
Byungjoo Kim ◽  
...  
Keyword(s):  
Dna Damage ◽  
Cell Death ◽  
Cancer Cells ◽  
Dna Damage Response ◽  
Transcriptional Activation ◽  
Metabolic Response ◽  
Apoptotic Cell ◽  
Glutamine Metabolism ◽  
Damage Response

AbstractThe DNA damage response is essential for sustaining genomic stability and preventing tumorigenesis. However, the fundamental question about the cellular metabolic response to DNA damage remains largely unknown, impeding the development of metabolic interventions that might prevent or treat cancer. Recently, it has been reported that there is a link between cell metabolism and DNA damage response, by repression of glutamine (Gln) entry into mitochondria to support cell cycle arrest and DNA repair. Here, we show that mitochondrial Gln metabolism is a crucial regulator of DNA damage-induced cell death. Mechanistically, inhibition of glutaminase (GLS), the first enzyme for Gln anaplerosis, sensitizes cancer cells to DNA damage by inducing amphiregulin (AREG) that promotes apoptotic cell death. GLS inhibition increases reactive oxygen species production, leading to transcriptional activation of AREG through Max-like protein X (MLX) transcription factor. Moreover, suppression of mitochondrial Gln metabolism results in markedly increased cell death after chemotherapy in vitro and in vivo. The essentiality of this molecular pathway in DNA damage-induced cell death may provide novel metabolic interventions for cancer therapy.

Inhibition of DNA damage response pathway using combination of DDR pathway inhibitors and radiation in treatment of acute lymphoblastic leukemia cells

2021 ◽  
Author(s):  
Maryam Katoueezadeh ◽  
Niloofar Pilehvari ◽  
Ahmad Fatemi ◽  
Gholamhossein Hassanshahi ◽  
Seyedeh Atekeh Torabizadeh
Keyword(s):  
Dna Damage ◽  
Acute Lymphoblastic Leukemia ◽  
Cancer Cells ◽  
Dna Damage Response ◽  
Therapeutic Strategy ◽  
Synergistic Effects ◽  
Lymphoblastic Leukemia ◽  
Treatment Strategies ◽  
Damage Response ◽  
Dna Damage Response Pathway

An alarming increase in acute lymphoblastic leukemia cases among children and adults has attracted the attention of researchers to discover new therapeutic strategies with a better prognosis. In cancer cells, the DNA damage response (DDR) pathway elements have been recognized to protect tumor cells from various stresses and cause tumor progression; targeting these DDR members is an attractive strategy for treatment of cancers. The inhibition of the DDR pathway in cancer cells for the treatment of cancers has recently been introduced. Hence, effective treatment strategies are needed for this purpose. Chemotherapy in combination with radiotherapy is considered a potential therapeutic strategy for acute leukemia. This review aims to assess the synergistic effects of these inhibitors with irradiation for the treatment of leukemia.

Evaluation of DNA Damage Response After Carbon-Ion Beam Irradiation in p53-Mutant Cancer Cells

2014 ◽  
Vol 90 (1) ◽  
pp. S786
Author(s):  
N. Amornwichet ◽  
T. Oike ◽  
M. Komachi ◽  
M. Isono ◽  
H. Ogiwara ◽  
...  
Keyword(s):  
Dna Damage ◽  
Cancer Cells ◽  
Dna Damage Response ◽  
Ion Beam ◽  
Beam Irradiation ◽  
Ion Beam Irradiation ◽  
Carbon Ion ◽  
Damage Response ◽  
Carbon Ion Beam

scholarly journals Depletion of the DarG antitoxin in Mycobacterium tuberculosis triggers the DNA‐damage response and leads to cell death

2020 ◽  
Vol 114 (4) ◽  
pp. 641-652 ◽  
Author(s):  
Anisha Zaveri ◽  
Ruojun Wang ◽  
Laure Botella ◽  
Ritu Sharma ◽  
Linnan Zhu ◽  
...  
Keyword(s):  
Dna Damage ◽  
Cell Death ◽  
Mycobacterium Tuberculosis ◽  
Dna Damage Response ◽  
Damage Response
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