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. 2022 Jul 26;13:4318. doi: 10.1038/s41467-022-32050-4

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© The Author(s) 2022, corrected publication 2022

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 3 — a Cartoon illustration of the MMP-2-triggered cleavage of the PEG corona and promoted cellular uptake of the PGD7 NPs in vitro. b Flow cytometric analysis of PGDA7 and PDA7 NPs cellular uptake in vitro (the NPs were pretreated with 0.2 mg/mL MMP-2 for 1 h) (n = 3 biologically independent cells). c CLSM examination of the intracellular distribution of the POLY-PROTAC NPs after 12 h of incubation (scale bar = 20 μm). d–f MMP-2-responsive PGDA7 NPs displayed increased penetration into MDA-MB-231 MCSs in vitro compared with their MMP-2-nonresponsive PDA7 counterpart. d CLSM examination of PGDA7 and PDA7 NPs distribution after 12 h of incubation in vitro. e 2.5-D reconstruction of the CLSM images at a scanning depth of 50 μm. f Fluorescence intensity of the central region versus Z-axis depth. g–j Reduction-activatable POLY-PROTAC NPs efficiently degraded the BRD4 protein in MDA-MB-231 cells in vitro. Western blot assay of BRD4 degradation in MDA-MB-231 cells with various GSH-sensitive POLY-PROTAC NPs in vitro after 24 h of incubation. k Western blot assay of BRD4 expression in PGDO7 NP-treated MDA-MB-231 cells in vitro. l DC₅₀ of the POLY-PROTAC NP-mediated degradation of BRD4 in MDA-MB-231 cells in vitro (n = 4 biologically independent cells). m POLY-PROTAC NPs degraded the POI via the ubiquitin-proteasome system. Western blot assay of BRD4 expression in MDA-MB-231 cells with or without MG132 incubation (MZ1/ARV771 concentrations of 1.0 μM and MG132 concentration of 5.0 mM). n PGDM and PGD7 NPs efficiently inhibited the proliferation of MDA-MB-231 cells in vitro (n = 4 biologically independent cells) (the POLY-PROTAC NPs were named according to the PROTAC and components integrated. P: PEG chain; G: GPLGLAG peptide; D: acid-activatable DPA group; 7: disulfide bond-bearing ARV771 methacrylate; M: disulfide bond-bearing MZ1 methacrylate; O7: ethylene group-bearing ARV771 methacrylate; A: PPa. See Supplementary Fig. 31 for NPs compositions). All data are presented as mean ± SD.