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. 2022 Feb 16;13:904. doi: 10.1038/s41467-022-28520-4

Fig. 3. Targeted degradation using AUTOTAC inactivates oncogenic signaling.

Fig. 3

a ICC of LNCaP cells treated with Vinclo.-2204 (2.5 µM, 24 h). Scale bar, 10 μm. b Quantification of (a) (n = 3 biologically independent experiments each counting 50 cells). c ICC of ACHN cells treated with PHTPP-1304 at the indicated concentrations and HCQ (10 μM) (24 h). Scale bar, 10 μm. d Quantification of (c) (n = 3 biologically independent experiments each counting 50 cells). e WB in U-87 MG cells treated with fumagillin-105 (1 μM, 24 h) with or without bafilomycin A1 (200 nM, 6 h). f WB in HEK293T cells treated with PHTPP-1304 (0.1 μM, 24 h) under siRNA-mediated knockdown of p62 and ATG5 (40 nM, 48 h). g WB in HeLa cells treated with fumagillin-105 (0.1 μM, 24 h) following RNA interference of Ubb (40 nM, 48 h). h Identical to (g), but with PHTPP-1304 for ERβ. i WB in LNCaP cells treated with vinclozolinM2-2204 (2.5 μM) or inclozolin (10 μM) with or without DHT (15 nM) (24 h). j Identical to (i) but with PHTPP-1304 (0.5 μM) or PHTPP (5 μM) with or without E2 (10 nM) (24 h). k Wound healing assay in ACHN cells treated with PHTPP-1304, PHTPP, or YOK-1304 (5 μM) at the indicated time points. l Quantification of (k) (n = 2 biologically independent experiments). Scale bar, 100 μm. m, n Cell viability assay of ACHN and LNCaP cells treated with the indicated compounds and concentrations (n = 2 biologically independent experiments). Data are presented as mean values ± SD where relevant. P-values (from a two-sided unpaired t test): ***P < 0.000276, **P < 0.00161. Source data are provided with this paper.