Identification of differentially expressed genes upon shRNA knockdown of TAL1 and its regulatory partners in T-ALL cells (Jurkat)

ABSTRACT: The oncogenic transcription factor TAL1/SCL is aberrantly overexpressed in over 40% of cases of T-cell acute lymphoblastic leukemia (T-ALL), emphasizing the importance of the TAL1-regulated transcriptional program in the molecular pathogenesis of T-ALL. Here we identify the core transcriptional regulatory circuit controlled by TAL1 and its regulatory partners HEB, E2A, GATA3, ETS1 and RUNX1 in T-ALL cells. We find that TAL1 forms an interconnected auto-regulatory loop with its partners, which contributes to the sustained upregulation of its direct target genes. Importantly, we also find the MYB oncogenic transcription factor is directly activated by the TAL1 complex and positively regulates many of the same target genes, thus forming a feed-forward positive regulatory loop that further promotes the TAL1-regulated oncogenic program. Two experiments were performed: 1. Duplicate hairpins for each transcription factor (TAL1, TCF12/HEB, TCF3/E2A, GATA3, MYB) and control hairpins (GFP and Luciferase) were used to idenfity the expression change in the T-ALL cell line (Jurkat) 2. Duplicate hairpins for RUNX1 and control hairpins (GFP and Luciferase) were used to idenfity the expression change in the T-ALL cell line (Jurkat)

ORGANISM(S): Homo sapiens

SUBMITTER: Richard Young 

PROVIDER: E-GEOD-29179 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress