Fig. 2: TG02 reduced the phosphorylation of RNA pol II, inhibited RNA synthesis and reduced Mcl-1 levels in CLL cells. | Blood Cancer Journal

Fig. 2: TG02 reduced the phosphorylation of RNA pol II, inhibited RNA synthesis and reduced Mcl-1 levels in CLL cells.

From: The multi-kinase inhibitor TG02 induces apoptosis and blocks B-cell receptor signaling in chronic lymphocytic leukemia through dual mechanisms of action

Fig. 2

A A representative immunoblot (n = 3) of the phosphorylation status of the Ser2 and Ser5 sites of RNA pol II CTD, Mcl-1, Bcl-2, Bcl-XL, and PARP in the CLL cells after a 4 and 24 h incubation with TG02 at 0.5, 1, and 2 μM, sunitinib (FLT3i) at 3 μM and TG-101348 (JAK2i) at 10 μM. Actin was used as a loading control. Cell viability was shown at the bottom of the blots. B Quantitation of the immunoblots of RNA pol II phosphorylation (Ser2, left; Ser5, right) at 4 h (●) and 24 h (◾) from 3 different CLL samples. Levels of phosphorylation were normalized to total RNA pol II and presented as percentage (mean ± SEM) of controls. C TG02 inhibited RNA synthesis in CLL cells. CLL cells were incubated with TG02 for 4 h (●) and 24 h (◾) and [3H]uridine incorporation was measured as described in “Methods”. The DPM values were normalized to time-matched controls and presented as mean ± SEM from three samples. D TG02 reduced the mRNAs of Mcl-1 (left) and Bcl-2 (right) in CLL cells after 4 h (●) and 24 h (◾) of incubation with TG02. E Quantitation of Mcl-1 and Bcl-2 proteins after 4 h (●) and 24 h (◾) of incubation with TG02 from three different CLL samples. Data were presented as percentage (mean ± SEM, n = 3) of controls.

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