Exploring redox vulnerabilities in JAK2^V617F-positive cellular models.

ABSTRACT:

Background

In Philadelphia chromosome-negative myeloproliferative neoplasm (MPN) models, reactive oxygen species (ROS) are elevated and have been implicated in genomic instability, JAK2/STAT signaling amplification, and disease progression. Although the potential effects of ROS on the MPN phenotype, the effects of ruxolitinib treatment on ROS regulation have been poorly explored. Herein, we have reported the impact of ruxolitinib on redox signaling transcriptional network, and the effects of diphenyleneiodonium (DPI), a pan NOX inhibitor, in JAK2^V617F-driven cellular models.

Method

Redox signaling-related genes were investigated in SET2 cells upon ruxolitinib treatment by RNA-seq (GEO accession GSE69827). SET2 and HEL cells, which represent JAK2^V617F-po

SUBMITTER: Lima K 

PROVIDER: S-EPMC8573030 | biostudies-literature | 2021 Oct-Dec

REPOSITORIES: biostudies-literature