Impaired MC3T3-E1 osteoblast differentiation triggered by oncogenic HRAS is rescued by the farnesyltransferase inhibitor Tipifarnib.

ABSTRACT: HRAS is a ubiquitously expressed protein and functions as a central regulator of cellular homeostasis. In somatic cells, mutations in this gene cause cancer, while germline mutations trigger a developmental disorder known as Costello syndrome (CS). Among numerous pathologies, adult CS patients develop osteoporosis. Previous studies revealed that HRAS is implicated in bone homeostasis by controlling osteoblast differentiation, adaptation to mechanical strain and repression of RANKL expression in mature osteoblasts, and by regulating osteoclast differentiation. However, the impact of HRAS on osteoblast differentiation is still debatable. In this study, we created stable doxycycline inducible cell lines overexpressing HRAS G12 mutants in MC3T3-E1 preosteoblast cell line and analyzed their imp

SUBMITTER: Andrasch Y 

PROVIDER: S-EPMC11861272 | biostudies-literature | 2025 Feb

REPOSITORIES: biostudies-literature