Figure - PMC

Skip to main content

An official website of the United States government

Here's how you know

Here's how you know

Official websites use .gov
A .gov website belongs to an official government organization in the United States.

Secure .gov websites use HTTPS
A lock ( ) or https:// means you've safely connected to the .gov website. Share sensitive information only on official, secure websites.

View full-text article in PMC

. 2019 Sep 20;10(10):695. doi: 10.1038/s41419-019-1950-1

Search in PMC
Search in PubMed
View in NLM Catalog
Add to search

© The Author(s) 2019

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/.

PMC Copyright notice

Fig. 1 — a MDA-MB231 cells express high level of mutated p53 (p53^R280K) lacking transcriptional activity as shown by the absence of p53-dependent transactivation of its target gene p21 even after γ-irradiation. b, c 24-48 h treatment with CP-31398 reactivates p53 transcriptional activity in MDA-MB231 cells as shown by induction of p21 expression at both mRNA (b) and protein (c) levels. d–f CP-31398-induced apoptosis and ROS production were evaluated after 48 h treatment using AnnexinV/PI (d, e) or DHE (f) staining. g, h CP-31398 treatment (48 h) increases MDA-MB231 cell susceptibility to NK-mediated lysis. ⁵¹Cr release assay using NK92 (d) or NK cells isolated from a healthy donor (e) co-cultured with target cells at different E:T ratios are shown. i CP-31398 treatment increases MDA-MB231 cell susceptibility to NK-mediated lysis in a time dependent manner. A representative ⁵¹Cr release assay (from two independent experiments) using NK cells isolated from a healthy donor is shown. j, k PFT-α (an inhibitor of p53 transcriptional activity) inhibits CP-31398-dependent induction of p21 expression in MDA-MB231 cells at both mRNA (j) and protein (k) levels. l, m PFT-α inhibits the increase of MDA-MB231 lysis by NK cells observed when CP-31398 is used alone. ⁵¹Cr release assay using NK92 (l) or NK cells extracted from a healthy donor (m) co-cultured with target cells at the E:T ratio of 50:1 or 30:1, respectively, are shown. n–p The knockdown of mutated p53 expression using siRNA inhibits CP-31398-dependent induction of p21 expression in MDA-MB231 cells at both mRNA (n) and protein (o) levels and abrogate the CP-31398-dependent increase of MDA-MB231 lysis by NK cells (p). Data are representative of at least three independent experiments (a, c, d, k, o) or are the mean ± s.d. of three (e–h, l, m, p) or five (b, j, n) independent experiments. The p values (*P < 0.05; **P < 0.01) were determined by unpaired two-tailed Student's t test (b, e, g, h, j, l–n) or one-way ANOVA (p)