RNA Shielding of p65 Is Required to Potentiate Oncogenic Inflammation in TET2-Mutated Clonal Hematopoiesis.

ABSTRACT:

Significance

This work identifies MALAT1 as a requisite downstream effector of oncogenic feedforward inflammatory circuits necessary for the development of TET2-mutated CH and fulminant myeloid malignancy. We elucidate a novel mechanism by which MALAT1 "shields" p65 from dephosphorylation to potentiate this circuit and nominate MALAT1 inhibition as a future therapeutic strategy.

SUBMITTER: Ben-Crentsil NA 

PROVIDER: S-EPMC11611684 | biostudies-literature | 2024 Dec

REPOSITORIES: biostudies-literature