Increased Protein Processing Gene Signature in HDACi-resistant cells predicts response to proteasome inhibitors.

ABSTRACT: Epigenetic modifying enzymes are commonly mutated in diffuse large B cell lymphoma (DLBCL). Importantly, genetics abnormalities lead to inactivation of HAT, which tilt the balance in favor of decreased protein acetylation in DLBCL cells. This suggests that protein acetylation regulation is an important factor in DLBCL pathogenesis and a potential target for therapy. We developed resistant cell lines to the histone deacetylase inhibitor (HDACi) vorinostat, in order to better define molecular mechanisms of action of HDACi in lymphoma cells. We found that cells resistant to HDACi have increased protein synthesis and proteasomal degradation. Additionally, cells resistant to HDACi have acquired increased susceptibility to proteasome inhibitors and this correlates with activation of the unfold

ORGANISM(S): Homo sapiens

SUBMITTER: Koren Mann 

PROVIDER: E-GEOD-58421 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress