Fig. 3: DCC-2036 decreases the KLF5 expression through the inhibition of AXL. | Cell Death & Disease

Fig. 3: DCC-2036 decreases the KLF5 expression through the inhibition of AXL.

From: Inhibitory effect of the novel tyrosine kinase inhibitor DCC-2036 on triple-negative breast cancer stem cells through AXL-KLF5 positive feedback loop

Fig. 3

A DCC-2036 inhibited the activation and expression of AXL in a dose-dependent manner. MDA-MB-231 cells, HS-578T, and 4T1 cells were treated with indicated concentrations of DCC-2036 for 48 h, and then the phosphorated and total levels of AXL were detected by WB. B Gas6 increased the protein levels of p-AXL and KLF5. MDA-MB-231 cells, HS-578T, and 4T1 cells were treated with Gas6 (200 ng/ml) for 0, 30, 60, 90, 120 min. C The knockdown of AXL reduced the protein levels of p-AXL, AXL, and KLF5. MDA-MB-231 cells were transfected with human AXL siRNA or control siRNA (NC) for 48 h, and then the protein levels were tested by WB. D The mRNA levels of AXL, KLF5, and Nanog were quantified by q RT-PCR. The statistical significance was determined by Student’s t-test, **P < 0.01. E The knockdown of both MET and P65 had no downregulation effect on KLF5. MDA-MB-231 cells were transfected with human MET siRNA/NC or P65 siRNA/NC for 48 h and then for WB assay. F MG132 reversed the decrease of KLF5 induced by AXL knockdown in MDA-MB-231 cells and HS-578T cells. The cells were transfected with AXL siRNA for 44 h and then were treated with MG132 (20 μM) for 4 h.

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