Fig. 5.

Resensitization of TAM via SN52-inhibited RelB nuclear translocation. (A) a SN52 peptide and its mutant control SN52 M with an acetylation (Ac) region for improving cell permeability were redesigned to inhibit RelB nuclear translocation. The Ac-region provided cell permeability, and the nuclear localization signal (NLS) was designed to compete with p52. The mutant NLS indicated in SN52 M served as a control. (B) Nuclear RelB levels in SN52-pretreated cells were imaged by confocal microscopy. (C) The levels of cytoplasmic and nuclear RelB in SN52-pretreated cells were measured by immunoblotting. (D) The effect of SN52 on enhanced TAM cytotoxicity was estimated by MTT assay (n = 4). (E, F) SN52 effect on cell survival in TAMS cells vs. TAMR cells was confirmed by colony survival assay (n = 3). (G, H) Furthermore, the SN52 effect on tumor growth was validated using a zebrafish xenograft tumor model (n = 10). Data are shown as mean ± SD, * (p < 0.05) and **(p < 0.01); two-way ANOVA.