Integral role of Noxa in p53-mediated apoptotic response

Shibue, Tsukasa; Takeda, Kiyoshi; Oda, Eri; Tanaka, Hiroshi; Murasawa, Hideki; Takaoka, Akinori; Morishita, Yasuyuki; Akira, Shizuo; Taniguchi, Tadatsugu; Tanaka, Nobuyuki

doi:10.1101/gad.1103603

Cited by 308 publications

(278 citation statements)

References 25 publications

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“…For example, Noxa and Puma are transcriptionally regulated by p53 and have been implicated in fibroblast anoikis [27,28]. Furthermore, in epithelial cells the Bcl-2 modifying factor (Bmf) behaves as sentinel able to register damage at the cytoskeleton and to convey a death signal.…”

Section: Intrinsic Pathwaymentioning

confidence: 99%

Anoikis: an emerging hallmark in health and diseases

Taddei

Giannoni

Fiaschi

et al. 2011

The Journal of Pathology

524

404

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Anoikis is a programmed cell death occurring upon cell detachment from the correct extracellular matrix, thus disrupting integrin ligation. It is a critical mechanism in preventing dysplastic cell growth or attachment to an inappropriate matrix. Anoikis prevents detached epithelial cells from colonizing elsewhere and is thus essential for tissue homeostasis and development. As anchorage-independent growth and epithelial-mesenchymal transition, two features associated with anoikis resistance, are crucial steps during tumour progression and metastatic spreading of cancer cells, anoikis deregulation has now evoked particular attention from the scientific community. The aim of this review is to analyse the molecular mechanisms governing both anoikis and anoikis resistance, focusing on their regulation in physiological processes, as well as in several diseases, including metastatic cancers, cardiovascular diseases and diabetes.

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Section: Intrinsic Pathwaymentioning

confidence: 99%

Anoikis: an emerging hallmark in health and diseases

Taddei

Giannoni

Fiaschi

et al. 2011

The Journal of Pathology

524

404

View full text Add to dashboard Cite

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“…EGL-1 induction plays a predominant role in DNA damage-induced apoptosis, while CED-13 appears to be important for UV-induced apoptosis (Schumacher et al 2005a ;Stergiou et al 2007 ) . Conceptually, the worm CEP-1 pathway acts analogously to the mammalian p53-dependent apoptosis induction of the BH3 proteins Puma and Noxa, which in turn leads to apoptosis induction analogous to EGL-1 by Bcl-2/CED-9 inactivation (Jeffers et al 2003 ;Villunger et al 2003 ;Shibue et al 2003 ;Oda et al 2000 ) . The cep-1 null mutant worms do not have any overt developmental or germline-speci fi c phenotype but are fully defective in DNA damage-induced apoptosis.…”

Section: Pathways Leading To Dna Damage-induced Apoptosismentioning

confidence: 99%

Germ Cell Apoptosis and DNA Damage Responses

Bailly

Gartner

2012

Advances in Experimental Medicine and Biology

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In the past 12 years, since the fi rst description of C. elegans germ cell apoptosis, this area of research rapidly expanded. It became evident that multiple genetic pathways lead to the apoptotic demise of germ cells. We are only beginning to understand how these pathways that all require the CED-9/Bcl-2, Apaf-1/CED-4 and CED-3 caspase core apoptosis components are regulated. Physiological apoptosis, which likely accounts for the elimination of more than 50% of all germ cells, even in unperturbed conditions, is likely to be required to maintain tissue homeostasis. The best-studied pathways lead to DNA damage-induced germ cell apoptosis in response to a variety of genotoxic stimuli. This apoptosis appears to be regulated similar to DNA damage-induced apoptosis in the mouse germ line and converges on p53 family transcription factors. DNA damage response pathways not only lead to apoptosis induction, but also directly affect DNA repair, and a transient cell cycle arrest of mitotic germ cells. Finally, distinct pathways activate germ cell apoptosis in response to defects in meiotic recombination and meiotic chromosome pairing.

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“…68 Studies have demonstrated that MEFs lacking PUMA or Noxa are resistant to DNA damage-induced apoptosis, a process known to be mediated by p53. [69][70][71] Another class of proapoptotic genes that can be regulated by p53, such as Fas or DR5/KILLER, are components of the apoptotic extrinsic pathway. 72 Finally, genes that encode redox-regulating enzymes such as the PIGs (p53-induced genes), which are involved in reactive oxygen species production, can damage the mitochondria, leading to apoptosis.…”

Section: Proapoptotic Bidmentioning

confidence: 99%

BCL2 family in DNA damage and cell cycle control

2006

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Individual BCL2 family members couple apoptosis regulation and cell cycle control in unique ways. Antiapoptotic BCL2 and BCL-x L are antiproliferative by facilitating G0. BAX is proapoptotic and accelerates S-phase progression. The dual functions in apoptosis and cell cycle are coordinately regulated by the multi-domain BCL2 family members (MCL-1) and suggest that survival is maintained at the expense of proliferation. The role of BH3-only molecules in cell cycle is more variable. BAD antagonizes both the cell cycle and antiapoptotic functions of BCL2 and BCL-x L through BH3 binding. BID has biochemically separable functions in apoptosis and S-phase checkpoint, determined by posttranslational modification. p53-induced PUMA is known only to have apoptotic function. Inhibition of apoptosis is oncogenic, whereas promotion of cell cycle arrest is tumor suppressive. Paradoxically, selected BCL2 family members can be both oncogenic and tumor suppressive. Which of the dual functions predominates is lineage specific and context dependent.

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Integral role of Noxa in p53-mediated apoptotic response

Cited by 308 publications

References 25 publications

Anoikis: an emerging hallmark in health and diseases

Anoikis: an emerging hallmark in health and diseases

Germ Cell Apoptosis and DNA Damage Responses

BCL2 family in DNA damage and cell cycle control

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