The lncRNA ELDR suppresses tumorigenicity of AML by interfering with DNA replication and chromatin accessibility.

ABSTRACT:

Abstract

Acute myeloid leukemia (AML) with rearrangement of the mixed lineage leukemia gene expresses MLL-AF9 fusion protein, a transcription factor that impairs differentiation and drives expansion of leukemic cells. In this work, the zinc finger protein "growth factor independent 1" together with the histone methyltransferase LSD1 is revealed to occupy the promoter and regulate the expression of the lncRNA ELDR (EGFR [epidermal growth factor receptor] long non-coding downstream RNA) in the rearranged Mixed Lineage Leukemia (MLL) (MLL-r) AML cell line THP-1. Forced ELDR overexpression enhanced the growth inhibition of an Lysine-Specific Demethylase 1 inhibitor (LSD1i)/all-trans retinoic acid (ATRA) combination treatment and reduced the capacity of these cells to generate leukemia

SUBMITTER: Arman K 

PROVIDER: S-EPMC12719172 | biostudies-literature | 2025 Dec

REPOSITORIES: biostudies-literature