Fig 1: CCRL2 knockdown affects the growth and clonogenicity of erythroleukemia cell lines.(A) CCRL2 knockdown with two different lentiviruses significantly suppresses the growth of TF-1 cells in the presence (P < 0.001) and absence of GM-CSF (P < 0.001). CCRL2 knockdown with two different lentiviruses suppresses at a lower extent the growth of DAMI cells (P = 0.009-sh1, P = 0.058-sh2). (B) CCRL2 knockdown with two different lentiviruses decreases the colony formation of TF-1 cells in the presence (P < 0.001) and absence of GM-CSF (P < 0.001). CCRL2 knockdown with two different lentiviruses decreases the colony formation of DAMI cells (P = 0.002-sh1, P = 0.015-sh2) at a lower extent compared with TF-1 cells. (C) CCRL2 knockdown with sh1 increased the percentage of apoptotic TF-1 cells (P = 0.015-sh1, P = 0.097-sh2), and CCRL2 knockdown with the two lentiviruses decreased the percentage of TF-1 cells in the G2-S phase (P < 0.001). (D) CCRL2 knockdown with two different lentiviruses increases the expression of CD41 (P < 0.001), CD71 (P < 0.001), and CD235a (P = 0.002-sh1, P = 0.025-sh2). CCRL2 knockdown does not affect the expression of CD41 (P = 0.230-sh1, P = 0.912-sh2). CCRL2 knockdown increases the expression of CD71 (P < 0.001-sh1, P = 0.026-sh2) and CD235a (P = 0.002-sh1, P = 0.067-sh2). (E) Western blotting showing the effect of CCRL2 knockdown in the JAK2/STAT signaling in TF-1 and DAMI cells. CCRL2 knockdown suppresses the phosphorylation of JAK2, STAT3, and STAT5 in TF-1 cells. CCRL2 knockdown decreases the phosphorylation of JAK2 but does not affect the phosphorylation of STAT3 and STAT5 in DAMI cells.