Fig. 3

The illustration indicates several pathways in AML cell: 1. CXCL-12/CXCR-4 axis initiates PI3K and ERK signaling pathways that leads to survival of AML cells through AKT and MAPK respectively. 2. Interaction of VEGFR-3 with its ligand (VEGF) starts PI3K/AKT/NO (survival), PI3K/BCL-2, Bag-1/Hsp, Ras/Raf (proliferation) and Ras/MKK (proliferation). 3. Several RTK ligands such as cytokines, growth factors, neurotropic factors, etc. interact with RTK that results in ERK/Ras (control of proliferation) ans p85/PDK1/AKT/mTOR. 4. some intracellular factors such as ROS and C-src are activated by GPCR. In the next step infiltration of these factors to cell membrane surface causes cleavage of proligands to ligand form of RTK. 5. HH ligands intract with PTCH. This interaction leads to inhibition of inhibitory activity of PTCH. When PTCH is inhibited, SMO can move toward the primary cillium and cause separation of GLI from SUFU. GLI in the nucleus promotes transcription of some target genes