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Table 2 Genes deregulated by MLL-AF9 and prioritized as potentially druggable targets in MLL-AF9 leukemia

From: RNAi-mediated silencing of MLL-AF9 reveals leukemia-associated downstream targets and processes

Gene

log2FC

Protein class

Official full name

Biological role

AHR

0.44

Nuclear receptor

Aryl hydrocarbon receptor

Upregulated by AML associated fusion gene AML1-ETO. Differentiation of myeloblastic leukemia cells. Estrogen receptor degradation. AHR knockout mice display CML.

ATP2B2

−0.69

Transporter

ATPase, Ca++ transporting, plasma membrane 2

Lowers intracellular calcium; protects from apoptosis.

DRD5

−0.96

Receptor

Dopamine receptor D5

Raised after G-CSF treatment; dopamine receptor agonists activate Wnt signaling, induce migration and increase clonogenic capacity and repopulation of CD34+ cells.

HIPK2

0.5

Enzyme

Homeodomain interacting protein kinase 2

Phosphorylates transcription (co-) factors (e.g. c-Myb); may trigger (myeloid) differentiation and apoptosis. Mutations found in AML cases.

PARP8

−0.63

Enzyme

Poly (ADP-ribose) polymerase family, member 8

Phosphorylated upon DNA damage. Upregulated in MLL rearranged AML patients.

ROR2

0.81

Receptor/enzyme

Receptor tyrosine kinase-like orphan receptor 2

Mediates noncanonical Wnt signaling. Putative tumor suppressor in leukemia, presumably via inhibition of Wnt canonical signaling.

TAS1R3

−2.01

Receptor

Taste receptor, type 1, member 3

Glucose absorption/energy supply. Heterodimers sense extracellular amino acids, activate MTORC1 and inhibit autophagy.

  1. Details to biological roles and references are given in Additional file 3: Table S2. Log2FC: log2 fold change in MLL-AF9 knockdown relative to control.