Atf3 deficiency promotes genome instability and spontaneous tumorigenesis in mice.

ABSTRACT: Mice lacking genes involving in the DNA-damage response (DDR) are often tumor prone owing to genome instability caused by oncogenic challenges. Previous studies demonstrate that activating transcription factor 3 (ATF3), a common stress sensor, can activate the tumor suppressor p53 and regulate expression of p53 target genes upon DNA damage. However, whether ATF3 contributes to the maintenance of genome stability and tumor suppression remains unknown. Here we report that Atf3-deficient (Atf3^-/-) mice developed spontaneous tumors, and died significantly earlier than wild-type (Atf3^+/+) mice. Consistent with these results, Atf3^-/- mouse embryonic fibroblasts (MEFs) had more aberrant chromosomes and micronuclei, and were genetically unstable. Whereas we demonst

SUBMITTER: Wang Z 

PROVIDER: S-EPMC6179156 | biostudies-literature | 2018 Jan

REPOSITORIES: biostudies-literature