Kras activation in p53-deficient myoblasts results in high-grade sarcoma formation with impaired myogenic differentiation.

ABSTRACT: While genomic studies have improved our ability to classify sarcomas, the molecular mechanisms involved in the formation and progression of many sarcoma subtypes are unknown. To better understand developmental origins and genetic drivers involved in rhabdomyosarcomagenesis, we describe a novel sarcoma model system employing primary murine p53-deficient myoblasts that were isolated and lentivirally transduced with KrasG12D. Myoblast cell lines were characterized and subjected to proliferation, anchorage-independent growth and differentiation assays to assess the effects of transgenic KrasG12D expression. KrasG12D overexpression transformed p53-/- myoblasts as demonstrated by an increased anchorage-independent growth. Induction of differentiation in parental myoblasts resulted in activation

SUBMITTER: McKinnon T 

PROVIDER: S-EPMC4546462 | biostudies-literature | 2015 Jun

REPOSITORIES: biostudies-literature