Fig. 6: ARID1A loss promotes MAP4 phosphorylation increasing EMP sensitivity.
From: MAP4 phosphorylation induced by ARID1A loss sensitizes colorectal cancer cells to EMP
The phosphorylated MAP4 levels in HCT116 (A) and RKO (B) ARID1A isogenic cell lines. Changes in protein expression level of PI3K/AKT signaling pathway in HCT116 (C) and RKO (D) ARID1A isogenic cell lines. Changes in protein expression level of PI3K/AKT signaling pathway induced by ARID1A silencing (E) or overexpression (F). G–I Interaction between MAP4 and PI3K. Co-immunoprecipitation assays were performed in HCT116 (G), RKO (H) and 293T (I) cell lines. J Changes of phosphorylated MAP4 expression level in HCT116 ARID1A isogenic cell pair treated with LY294002 (PI3K inhibitor). Microtubule polymerization status (K) and quantification of polymeric microtubules (L) in HCT116 ARID1A isogenic cell pair treated with EMP and LY294002, n = 3. P and S represent polymeric and soluble fractions of tubulin, respectively. Data are presented as mean ± SEM. **P < 0.01, Student’s t test.
