Sustained p16^INK4a expression is required to prevent IR-induced tumorigenesis in mice.

ABSTRACT: Exposure of murine and human tissues to ionizing radiation (IR) induces the expression of p16^INK4a, a tumor suppressor gene and senescence/aging biomarker. Increased p16^INK4a expression is often delayed several weeks post exposure to IR. In this context, it remains unclear if it occurs to suppress aberrant cellular growth of potentially transformed cells or is simply a result of IR-induced loss of tissue homeostasis. To address this question, we used a conditional p16^INK4a null mouse model and determined the impact of p16^INK4a inactivation long-term post exposure to IR. We found that, in vitro, bone marrow stromal cells exposed to IR enter DNA replication following p16^INK4a inactivation. However, these cells did not resume growth; inst

SUBMITTER: Palacio L 

PROVIDER: S-EPMC5336385 | biostudies-literature | 2017 Mar

REPOSITORIES: biostudies-literature