Apoptosis: Reprogramming and the Fate of Mature Cells

Cheung, Hoi‐Hung; Liu, Xiaozhuo; Rennert, Owen M.

doi:10.5402/2012/685852

Cited by 33 publications

(25 citation statements)

References 66 publications

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“…The increasing of ROS inhibited the survival of reprogramming cells which led to DNA damages, cellular senescence and apoptosis [7]. Thus, the factor which regulates ROS homeostasis may play a critical role for efficient reprogramming [7]. We showed that ROS production is higher in Jdp2 KO MEFs than in WT MEFs and that addition of an oxidative stress inducing reagent increased ROS production in Jdp2 KO MEFs compared with WT KO MEFs (Figure 1).…”

Section: Discussionmentioning

confidence: 94%

“…During reprogramming, Yamanaka factors induced the chromatin changes to generate the stress response including ROS production [50]. The increasing of ROS inhibited the survival of reprogramming cells which led to DNA damages, cellular senescence and apoptosis [7]. Thus, the factor which regulates ROS homeostasis may play a critical role for efficient reprogramming [7].…”

Section: Discussionmentioning

confidence: 99%

“…Many antioxidant and/or detoxification enzymes, such as NADPH: quinone oxidoreductase 1 (NQO1) [3,4], glutathione S -transferase (GST) [5], and heme oxygenase-1 (HO-1) [6] contribute to cellular defenses systems against ROS. The coordinated induction of the genes encoding the Phase II detoxification and antioxidant enzymes is governed by the core sequence 5'-G/A TGACNNNGC-3' located in their gene regulatory regions, and is termed the antioxidant responsive element (ARE) [7]. Nuclear factor-erythroid 2-related factor 2 (Nrf2) is the key factor responsible for binding to AREs.…”

Section: Introductionmentioning

confidence: 99%

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Control of Oxidative Stress and Generation of Induced Pluripotent Stem Cell-like Cells by Jun Dimerization Protein 2

Chiou

Wang

et al. 2013

Cancers

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We report here that the Jun dimerization protein 2 (JDP2) plays a critical role as a cofactor for the transcription factors nuclear factor-erythroid 2-related factor 2 (Nrf2) and MafK in the regulation of the antioxidants and production of reactive oxygen species (ROS). JDP2 associates with Nrf2 and MafK (Nrf2-MafK) to increase the transcription of antioxidant response element-dependent genes. Oxidative-stress-inducing reagent led to an increase in the intracellular accumulation of ROS and cell proliferation in Jdp2 knock-out mouse embryonic fibroblasts. In Jdp2-Cre mice mated with reporter mice, the expression of JDP2 was restricted to granule cells in the brain cerebellum. The induced pluripotent stem cells (iPSC)-like cells were generated from DAOY medulloblastoma cell by introduction of JDP2, and the defined factor OCT4. iPSC-like cells expressed stem cell-like characteristics including alkaline phosphatase activity and some stem cell markers. However, such iPSC-like cells also proliferated rapidly, became neoplastic, and potentiated cell malignancy at a later stage in SCID mice. This study suggests that medulloblastoma cells can be reprogrammed successfully by JDP2 and OCT4 to become iPSC-like cells. These cells will be helpful for studying the generation of cancer stem cells and ROS homeostasis.

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Section: Discussionmentioning

confidence: 94%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Control of Oxidative Stress and Generation of Induced Pluripotent Stem Cell-like Cells by Jun Dimerization Protein 2

Chiou

Wang

et al. 2013

Cancers

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“…Apoptosis is a tightly controlled mode of cell death that eliminates harmful cells upon treatment with anti-cancer drugs. It is morphologically characterized by chromatin condensation, cellular shrinkage, plasma membrane blebbing and nuclear fragmentation (Cheung et al, 2012;Pulido and Parrish, 2003). During apoptosis, a group of cysteine proteases, caspases, which contain a nucleophilic cysteine residue are activated and specifically cleave their substrate proteins after aspartic acid (Strasser et al, 2000).…”

Section: Introductionmentioning

confidence: 99%

Spiroquinazolinone-induced cytotoxicity and apoptosis in K562 human leukemia cells: alteration in expression levels of Bcl-2 and Bax

et al. 2015

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-Spiroquinazolinone compounds have been considered as a new series of potent apoptosis-inducing agents. In this study, anti-proliferative and apoptotic effects of the derivatives from the spiroquinazolinone family were investigated in the human chronic myeloid leukemia K562 cells. The K562 cells were treated with various concentrations of the spiroquinazolinone (10-300 μM) for 3 days and cell viability was determined by MTT growth inhibition assay. 4t-QTC was more active among these compounds with IC50 of 50 ± 3.6 μM and was selected for further studies. Apoptosis, as the mechanism of cell death was investigated morphologically by acridine orange/ethidium bromide (AO/EtBr) double staining, cell surface expression assay of phosphatidyl serine by Annexin V/PI technique, as well as the formation of DNA ladder. The K562 cells underwent apoptosis upon a single dose (at IC50 value) of the 4t-QTC compound, and over-expressed caspase-3 expression by more than 1.7-fold, following a 72 hr treatment. Furthermore, RT-PCR and Western blot analysis revealed that treatment of the K562 cells with 4t-QTC down-regulates and up-regulates the expression of Bcl-2 (anti-apoptotic) and Bax (pro-apoptotic), respectively. Based on the present data, it seems that these compounds from the spiroquinazolinone family are good candidates for further evaluation as an effective chemotherapeutic family acting through induction of apoptosis in chronic myeloid leukemia.

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“…(Cheung et al, 2012). In physiology, it plays a crucial role particularly during embryogenesis and metamorphosis.…”

Section: Introductionmentioning

confidence: 99%

Apoptosis in Cancer - An Update

Sankari¹,

Masthan²,

Babu³

et al. 2012

Asian Pacific Journal of Cancer Prevention

103

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Apoptosis is programmed cell death which is essential for development and survival of living organisms. It is a sequentially regulated suicidal programme where cells activate certain enzymes which dissolute their own nuclear component and various protein component of nucleus and cytoplasm. Disturbance of this regulatory pathway may lead to various diseases like autoimmune diseases, neurodegenerative diseases and cancers. The potential mechanisms of apoptosis and its role in cancer are discussed. The ability of apoptosis to modulate the life or death of a cell is also recognized for its immense therapeutic potential. Understanding the mechanisms from this review will give us better insight to the pathogenesis of various diseases including cancer and will open new horizons to therapeutic approaches.

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Apoptosis: Reprogramming and the Fate of Mature Cells

Cited by 33 publications

References 66 publications

Control of Oxidative Stress and Generation of Induced Pluripotent Stem Cell-like Cells by Jun Dimerization Protein 2

Control of Oxidative Stress and Generation of Induced Pluripotent Stem Cell-like Cells by Jun Dimerization Protein 2

Spiroquinazolinone-induced cytotoxicity and apoptosis in K562 human leukemia cells: alteration in expression levels of Bcl-2 and Bax

Apoptosis in Cancer - An Update

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