A redox cycle within the cell cycle: ring in the old with the new

Menon, Sarita G.; Goswami, Prabhat C.

doi:10.1038/sj.onc.1209895

Cited by 263 publications

(224 citation statements)

References 91 publications

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“…Values not sharing a common letter are significantly different at p \ 0.05 by TukeyKramer multiple comparisons test the treatment with pterostilbene could significantly increase the intracellular ROS level of the cells as early as 2 h after treatment. The fluctuations in the intracellular redox state during cell cycle progression could represent a fundamental mechanism linking oxidative metabolic processes to cell cycle regulatory processes (Menon and Goswami 2007).…”

Section: Resultsmentioning

confidence: 99%

Anti-proliferative effect of pterostilbene on rat hepatoma cells in culture

2014

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Pterostilbene, a methoxylated analogue of resveratrol, is a natural compound primarily found in blueberries and several types of grapes. However, little is known about the effect of pterostilbene on the proliferation of hepatoma cells and its modes of actions. This study was undertaken to characterize its ability to suppress the proliferation of hepatoma AH109A cells and the possible mechanism(s) involved. Pterostilbene showed a significant and dose-dependent effect on the anti-proliferative activity against AH109A cells. Pterostilbene exerted little or no effect on the proliferation of rat L6 myoblasts and rat skin fibroblasts. Pterostilbeneloaded rat sera could significantly inhibit the proliferation of AH109A cells, which suggests that pterostilbene could be absorbed through gastrointestinal tract and retain its anti-proliferative activity. Pterostilbene arrested the cell cycle of AH109A cells at G0/ G1 phase and reduced the protein expression of cyclindependent kinase 4 and cyclin-dependent kinase 6 dose-dependently. We also found that pterostilbene could significantly increase the intracellular peroxide level of AH109A cells, which may be involved in its anti-proliferative activity.

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Section: Resultsmentioning

confidence: 99%

Anti-proliferative effect of pterostilbene on rat hepatoma cells in culture

2014

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“…ROS were traditionally thought of as toxic byproducts in cells, which damaged cellular macromolecules and led cells to apoptosis (Shackelford et al, 1999). However, in recent years, several studies have shown that ROS can function as signaling molecules that regulate numerous cellular processes, including proliferation (Sundaresan et al, 1995;Behrend et al, 2003;Menon and Goswami, 2007;Bartosz, 2009). This dual function of ROS is based on differences in their concentrations, pulse duration and subcellular localization (Laurent et al, 2005;Bartosz, 2009).…”

Section: Discussionmentioning

confidence: 99%

“…This dual function of ROS is based on differences in their concentrations, pulse duration and subcellular localization (Laurent et al, 2005;Bartosz, 2009). High concentration of ROS in G1/S phase led to cell senescence or apoptosis and, on the contrary, low ROS facilitated cell cycle progression and activation of cell cycle regulators, such as, CDK4/6, cyclin D1, RB, p21 and E2F1 (Laurent et al, 2005;Menon and Goswami, 2007;Sarsour et al, 2009). The cell cycle regulation involved in the enhancement of proliferation seems to be mediated by the increase in phosphorylation and thiol-redox reaction induced by many mitochondrial proteins, such as MnSOD (Sakamaki et al, 2006;.…”

Section: Discussionmentioning

confidence: 99%

Functional interaction of Ugene and EBV infection mediates tumorigenic effects

et al. 2011

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Epstein-Barr virus (EBV) infection is associated with many human neoplasms, in which EBV-derived latent membrane protein-1 (LMP1) appears to be critical, but its exact oncogenic mechanism remains to be defined. To this end, our initial microarray analyses identified a LMP1-inducible gene, Ugene, originally characterized as a binding partner for uracil DNA glycosylase 2, which is highly expressed in malignant colon cancer. In this report, it was found that Ugene, designated herein as LMP1-induced protein (LMPIP), was induced, in a time-dependent manner, in EBV-infected peripheral blood mononuclear cells and LMP1-transfected 293 cells. Functionally, when compared with mock-transfected cells, overexpression of LMPIP in nasopharyngeal carcinoma (NPC) cell lines resulted in a decrease in reactive oxygen species production and maintained mitochondria membrane potential (Dw) loss induced by H 2 O 2 . The NPC cells transfected with LMPIP also showed a decrease in G1 population and an increase in the cell population in sub-G1 and multiploid phase, concomitant with increased levels of cell cycle activators, including cyclin D1 and CDK4. In contrast, silencing of LMPIP expression in the NPC tumor cell lines with short hairpin RNA interference revealed significantly decreased cell population at G1/S phase, while the number of cells in multiploid phase increased. Significantly, NPC cells with LMPIP knock-down also showed a decrease in tumorigenic and transforming activity induced by ectopic LMP1 expression, as determined by analyses of soft agar foci and tumor size in nude mice. Further, elevated LMPIP expression was also noted in cytoplasm and nuclei in EBVinfected NPC tumor cell mass and non-EBV-infected tumor cell lines. These results suggested that LMPIP may have an important mediator role in EBV-mediated neoplasm and may serve as a new target for therapy of tumors induced by EBV infection.

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“…Cell cycle progression in animals is considered to be driven by an intrinsic redox cycle consisting of reductive and oxidative phases (81)(82)(83)(84)(85). The binding of growth factors, such as epidermal growth factor (EGF) to their receptors (such as EGFR) is facilitated by ROS generation leading to oxidation and activation of signaling pathways that trigger cell proliferation (85).…”

Section: Gsh Is Required For the Cell Cycle In Rootsmentioning

confidence: 99%

Glutathione – linking cell proliferation to oxidative stress

Díaz‐Vivancos

Simone

Kiddle³

et al. 2015

Free Radical Biology and Medicine

291

177

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Significance:The multifaceted functions of reduced glutathione (gamma-glutamyl-cysteinyl-glycine; GSH) continue to fascinate plants and animal scientists, not least because of the dynamic relationships between GSH and reactive oxygen species (ROS) that underpin reduction/oxidation (redox) regulation and signalling. Here we consider the respective roles of ROS and GSH in the regulation of plant growth, with a particular focus on regulation of the plant cell cycle. Glutathione is discussed not only as a crucial low molecular weight redox buffer that shields nuclear processes against oxidative challenge but also a flexible regulator of genetic and epigenetic functions. Recent Advances:The intracellular compartmentalization of GSH during the cell cycle is remarkably consistent in plants and animals. Moreover, measurements of in vivo glutathione redox potentials reveal that the cellular environment is much more reducing than predicted from GSH/GSSG ratios measured in tissue extracts. The redox potential of the cytosol and nuclei of non-dividing plant cells is about -300 mV. This relatively low redox potential is maintained even in cells experiencing oxidative stress by a number of mechanisms including vacuolar sequestration of GSSG. We propose that regulated ROS production linked to glutathione-mediated signalling events are the hallmark of viable cells within a changing and challenging environment. Critical Issues:The concept that the cell cycle in animals is subject to redox controls is well established but little is known about how ROS and GSH regulate this process in plants. However, it is increasingly likely that similar redox controls exist in plants, 3 although possibly through different pathways. Moreover, redox-regulated proteins that function in cell cycle checkpoints remain to be identified in plants. While GSHresponsive genes have now been identified, the mechanisms that mediate and regulate protein glutathionylation in plants remain poorly defined.Future Directions: The nuclear GSH pool provides an appropriate redox environment for essential nuclear functions. Future work will function on how this essential thiol interacts with the nuclear thioredoxin system and nitric oxide to regulate genetic and epigenetic mechanisms. The characterization of redox-regulated cell cycle proteins in plants, and the elucidation of mechanisms that facilitate GSH accumulation in the nucleus are keep steps to unravelling the complexities of nuclear redox controls.Diaz 4

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A redox cycle within the cell cycle: ring in the old with the new

Cited by 263 publications

References 91 publications

Anti-proliferative effect of pterostilbene on rat hepatoma cells in culture

Anti-proliferative effect of pterostilbene on rat hepatoma cells in culture

Functional interaction of Ugene and EBV infection mediates tumorigenic effects

Glutathione – linking cell proliferation to oxidative stress

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