Fig. 6

Inhibition of the proteasome-induced protein degradation stabilizes β-catenin in chemotherapy-treated WAVE3-deficient cells. A–D Representative Western blots of protein lysates from WAVE3-deficient MDA-MB-231 (MDA-MB-231-W3KO) (A), WAVE3-deficient 231 cells overexpressing phospho-mutant WAVE3 (231-W3KO-W3Y4) (B), WAVE3-deficient 4T1 (4T1-W3KO) or WAVE3-deficient and (C) or WAVE3-deficient 4T1 cells overexpressing phospho-mutant WAVE3 (4T1-W3KO-W3Y4) cells (D) that were treated for 24 h with 0.1% DMSO, 10 µM cisplatin (Cis), 1 µM GM6001 (GM), or both GM6001 and cisplatin (GM + Cis), and were subjected to immunoblotting with antibodies against β-Catenin. β-Actin was used as loading control. E & F Representative Western blots of nuclear (E) or cytoplasmic (F) fraction of protein lysates from MDA-MB-231-W3KO cells that were treated for 24 h with 0.1% DMSO, 10 µM cisplatin (Cis), 1 µM GM6001 (GM), or both GM6001 and cisplatin (GM + Cis), were subjected to immunoblotting with antibodies against β-Catenin. α-Tubulin and Lamin B1 were used as loading controls for the nuclear and the cytoplasmic fraction, respectively. The numbers under each WB band represent the fold change in signal intensity with respect to its respective control band in each panel after normalization to the loading control signal. Data shown are representative of 3 replicates