ROS production by adrenodoxin does not cause apoptosis in fission yeast

Derouet-Hümbert, Evi; Drăgan, Călin-Aurel; Hakki, Tarek; Bureik, Matthias

doi:10.1007/s10495-007-0133-1

Cited by 14 publications

(3 citation statements)

References 32 publications

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“…31 Similar studies have shown that ROS are also produced in cells undergoing apoptotic-like cell death, but that the produced ROS do not cause apoptosis. 32 In this study, we observed that ROS were not required to induce apoptosis in PTEN-proficient glioma.…”

Section: Discussionmentioning

confidence: 61%

PTEN status switches cell fate between premature senescence and apoptosis in glioma exposed to ionizing radiation

et al. 2010

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Loss of the tumor suppressor phosphatase and tensin homolog (PTEN) has frequently been observed in human gliomas, conferring AKT activation and resistance to ionizing radiation (IR) and drug treatments. Recent reports have shown that PTEN loss or AKT activation induces premature senescence, but many details regarding this effect remain obscure. In this study, we tested whether the status of PTEN determined fate of the cell by examining PTEN-deficient U87, U251, and U373, and PTEN-proficient LN18 and LN428 glioma cells after exposure to IR. These cells exhibited different cellular responses, senescence or apoptosis, depending on the PTEN status. We further observed that PTEN-deficient U87 cells with high levels of both AKT activation and intracellular reactive oxygen species (ROS) underwent senescence, whereas PTEN-proficient LN18 cells entered apoptosis. ROS were indispensable for inducing senescence in PTEN-deficient cells, but not for apoptosis in PTENproficient cells. Furthermore, transfection with wild-type (wt) PTEN or AKT small interfering RNA induced a change from premature senescence to apoptosis and depletion of p53 or p21 prevented IR-induced premature senescence in U87 cells. Our data indicate that PTEN acts as a pivotal determinant of cell fate, regarding senescence and apoptosis in IR-exposed glioma cells. We conclude that premature senescence could have a compensatory role for apoptosis in the absence of the tumor suppressor PTEN through the AKT/ROS/p53/p21 signaling pathway.

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Section: Discussionmentioning

confidence: 61%

PTEN status switches cell fate between premature senescence and apoptosis in glioma exposed to ionizing radiation

et al. 2010

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“…ROS may also serve as cell signaling molecules and cause damage to foreign bodies (37). Overproduction of ROS may be induced by a number of intra-and extracellular stressors (38)(39)(40). In the present study, the production of ROS in Aloin-treated A549 cells was evaluated.…”

Section: Discussionmentioning

confidence: 94%

Aloin promotes A549 cell apoptosis via the reactive oxygen species-mitogen activated protein kinase signaling pathway and p53 phosphorylation

Wan

Zhang

Fan

et al. 2017

Molecular Medicine Reports

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Aloin has the potential to be a novel anticancer agent in cancer therapies. However, the detailed anticancer effect of Aloin remains to be fully elucidated. The present study analyzed the p53‑dependent mechanisms in response to Aloin treatment. Using the p53‑proficient A549 cells, an Aloin‑induced apoptotic cell model was established, which was used to evaluate the potential underlying molecular mechanisms. The results demonstrated that 200, 300 and 400 µM Aloin induced intrinsic cell apoptosis, which was further confirmed by disruption of the mitochondrial membrane potential, elevation of cytosolic Ca2+ levels, and activation of B‑cell lymphoma 2 (Bcl‑2) homologous antagonist killer, Bcl‑2 X‑associated protein, p53 upregulated modulator of apoptosis and phorbol‑12‑myristate‑13‑acetate‑induced protein 1. Aloin‑induced apoptosis was also accompanied by the induction of p53 phosphorylation on Serine (Ser)15, Threonine 18, Ser20 and Ser392; however, there were no significant differences in the expression of p53 and mouse double minute 2 homolog. Aloin‑induced apoptosis was reactive oxygen species (ROS)‑ and c‑Jun/p38‑dependent, as specific inhibitors for ROS, phosphorylated (p)‑c‑Jun and p‑p38 may attenuate Aloin‑induced A549 cell proliferating inhibition. In conclusion, these results suggested that Aloin may induce apoptosis in A549 cells via the ROS‑mitogen activated protein kinase signaling pathway, with p53 phosphorylation. These results implicate Aloin as a potential therapeutic agent for the treatment of lung cancer.

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“… 103 Interestingly, recombinant expression of Adx does not cause apoptosis in the microbial model system Schizosaccharomyces pombe , in spite of a strong increase in ROS, which is indeed much higher than that observed in mammalian cells. 114 An explanation for this observation might well be connected to the very recent finding that S. pombe , in contrast to baker’s yeast ( Saccharomyces cerevisiae ), does not age. 115 …”

Section: Cytochrome P450 Enzymesmentioning

confidence: 99%

Bystander signaling via oxidative metabolism

Sawal¹,

Asghar²,

Bureik³

et al. 2017

OTT

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The radiation-induced bystander effect (RIBE) is the initiation of biological end points in cells (bystander cells) that are not directly traversed by an incident-radiation track, but are in close proximity to cells that are receiving the radiation. RIBE has been indicted of causing DNA damage via oxidative stress, besides causing direct damage, inducing tumorigenesis, producing micronuclei, and causing apoptosis. RIBE is regulated by signaling proteins that are either endogenous or secreted by cells as a means of communication between cells, and can activate intracellular or intercellular oxidative metabolism that can further trigger signaling pathways of inflammation. Bystander signals can pass through gap junctions in attached cell lines, while the suspended cell lines transmit these signals via hormones and soluble proteins. This review provides the background information on how reactive oxygen species (ROS) act as bystander signals. Although ROS have a very short half-life and have a nanometer-scale sphere of influence, the wide variety of ROS produced via various sources can exert a cumulative effect, not only in forming DNA adducts but also setting up signaling pathways of inflammation, apoptosis, cell-cycle arrest, aging, and even tumorigenesis. This review outlines the sources of the bystander effect linked to ROS in a cell, and provides methods of investigation for researchers who would like to pursue this field of science.

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ROS production by adrenodoxin does not cause apoptosis in fission yeast

Cited by 14 publications

References 32 publications

PTEN status switches cell fate between premature senescence and apoptosis in glioma exposed to ionizing radiation

PTEN status switches cell fate between premature senescence and apoptosis in glioma exposed to ionizing radiation

Aloin promotes A549 cell apoptosis via the reactive oxygen species-mitogen activated protein kinase signaling pathway and p53 phosphorylation

Bystander signaling via oxidative metabolism

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