AustralieFrV1, Main, Exploration, bibRecord, 005B73

INT6/EIF3E Interacts with ATM and Is Required for Proper Execution of the DNA Damage Response in Human Cells

Identifieur interne : 005B73 ( Main/Exploration ); précédent : 005B72; suivant : 005B74

INT6/EIF3E Interacts with ATM and Is Required for Proper Execution of the DNA Damage Response in Human Cells

Auteurs : Christelle Morris [France] ; Nozomi Tomimatsu [États-Unis] ; Derek J. Richard [Australie] ; David Cluet [France] ; Sandeep Burma [États-Unis] ; Kum Kum Khanna [Australie] ; Pierre Jalinot [France]

Source :

Cancer research : (Baltimore) [ 0008-5472 ] ; 2012.

RBID : Pascal:12-0198170

Descripteurs français

Pascal (Inist)
- Gène suppresseur tumeur, Homme, In vitro, Cellule, Gène ATM, Réponse à une lésion d'ADN.
Wicri :
- topic : Homme.

English descriptors

KwdEn :
- Cell, DNA damage response, Human, In vitro, Tumor suppressor gene.

Abstract

Altered expression of the INT6 gene, encoding the e subunit of the translational initiation factor eIF3, occurs in human breast cancers, but how INT6 relates to carcinogenesis remains unestablished. Here, we show that INT6 is involved in the DNA damage response. INT6 was required for cell survival following γ-irradiation and G₂-M checkpoint control. RNA interference-mediated silencing of INT6 reduced phosphorylation of the checkpoint kinases CHK1 and CHK2 after DNA damage. In addition, INT6 silencing prevented sustained accumulation of ataxia telangiectasia mutated (ATM) at DNA damage sites in cells treated with γ-radiation or the radiomimetic drug neocarzinostatin. Mechanistically, this result could be explained by interaction of INT6 with ATM, which together with INT6 was recruited to the sites of DNA damage. Finally, INT6 silencing also reduced ubiquitylation events that promote retention of repair proteins at DNA lesions. Accordingly, accumulation of the repair factor BRCA1 was defective in the absence of INT6. Our findings reveal unexpected and striking connections of INT6 with ATM and BRCA1 and suggest that the protective action of INT6 in the onset of breast cancers relies on its involvement in the DNA damage response.

Url:

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3335344

Affiliations:

Australie, France, États-Unis
Auvergne-Rhône-Alpes, Rhône-Alpes, Texas
Dallas, Lyon

Le document en format XML

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<front><div type="abstract" xml:lang="en">Altered expression of the INT6 gene, encoding the e subunit of the translational initiation factor eIF3, occurs in human breast cancers, but how INT6 relates to carcinogenesis remains unestablished. Here, we show that INT6 is involved in the DNA damage response. INT6 was required for cell survival following γ-irradiation and G<sub>2</sub>
-M checkpoint control. RNA interference-mediated silencing of INT6 reduced phosphorylation of the checkpoint kinases CHK1 and CHK2 after DNA damage. In addition, INT6 silencing prevented sustained accumulation of ataxia telangiectasia mutated (ATM) at DNA damage sites in cells treated with γ-radiation or the radiomimetic drug neocarzinostatin. Mechanistically, this result could be explained by interaction of INT6 with ATM, which together with INT6 was recruited to the sites of DNA damage. Finally, INT6 silencing also reduced ubiquitylation events that promote retention of repair proteins at DNA lesions. Accordingly, accumulation of the repair factor BRCA1 was defective in the absence of INT6. Our findings reveal unexpected and striking connections of INT6 with ATM and BRCA1 and suggest that the protective action of INT6 in the onset of breast cancers relies on its involvement in the DNA damage response.</div>
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INT6/EIF3E Interacts with ATM and Is Required for Proper Execution of the DNA Damage Response in Human Cells

INT6/EIF3E Interacts with ATM and Is Required for Proper Execution of the DNA Damage Response in Human Cells

Source :

Descripteurs français

English descriptors

Abstract

Links toward previous steps (curation, corpus...)

Le document en format XML

Pour manipuler ce document sous Unix (Dilib)

Pour mettre un lien sur cette page dans le réseau Wicri

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