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INT6/EIF3E interacts with ATM and is required for proper execution of the DNA damage response in human cells

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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 [ 0008-5472 ] ; 2012.

RBID : PMC:3335344

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. RNAi-mediated silencing of INT6 reduced phosphorylation of the checkpoint kinases CHK1 and CHK2 after DNA damage. Additionally, INT6 silencing prevented sustained accumulation of 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 sites of DNA damage. Lastly, 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

DOI: 10.1158/0008-5472.CAN-11-2562
PubMed: 22508697
PubMed Central: 3335344

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PMC:3335344

Le document en format XML

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<front><div type="abstract" xml:lang="en"><p id="P1">Altered expression of the <italic>INT6</italic>
 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. RNAi-mediated silencing of INT6 reduced phosphorylation of the checkpoint kinases CHK1 and CHK2 after DNA damage. Additionally, INT6 silencing prevented sustained accumulation of 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 sites of DNA damage. Lastly, 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.</p>
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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 :

Abstract

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

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Le document en format XML

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