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. 2021 Feb 18;107(1):143–153. doi: 10.3324/haematol.2020.263756

Figure 4.

Figure 4.

The TGFbR pathway is deregulated in T-cell prolymphocytic leukemia. (A) Overexpression of miR-200c and miR-141 relative to U6 in HeLa-Mir-200c/141 compared to HeLa-empty vector (EV) is plotted. (B) The mRNA expression of ZEB2 and TGFbR3 relative to GAPDH in HeLa-Mir-200c/141 compared to HeLa-EV is plotted. (C) HeLa-Mir-200c/141 and HeLa-EV cells were treated with hu-TGFb1 (10 ng/mL, +) or not stimulated (0 ng/mL, - hu-TGFb1) for 1 hour. Samples of cell lysates were taken and analyzed by western blotting using phospho-specific antibodies against SMAD2 and SMAD3, total SMAD2/3, b-actin and TGFβR1. Data are representative of three independent experiments. (D) Cells were stimulated with hu-TGFb1 (+ hu-TGFb1) or not stimulated (0 ng/mL, - hu-TGFβ1) for 1 hour. Samples of indicated cell lysates were analyzed by western blotting with phospho-specific antibodies against SMAD2 and SMAD3, total SMAD (SMAD2 = upper band, SMAD3 = lower band) and β-actin. (E) Quantification of the data shown in (D). Induction of hu-TGFb1-mediated phosphorylation of indicated phospo-proteins relative to the total SMAD expression level and peripheral blood mononuclear cells (PBMC) values of the different samples are depicted.