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

. 2022 Jul 8;13(7):590. doi: 10.1038/s41419-022-05023-0

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

© The Author(s) 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/.

PMC Copyright notice

Fig. 7 — A Both NONO and SAMHD1 were upregulated in AML-resistant cells compared with the corresponding parental cells. The protein levels of NONO and SAMHD1 in HL60-R and HEL-R cells and the corresponding parental cells were evaluated by western blotting (P indicates parental cells. HL60-R-4 μM and HL60-R-8 μM, HEL-R-4 μM, and HEL-R-8 μM indicate the maximum sustained concentrations of Ara-C used for culture of the resistant AML cell lines). B Silencing NONO restored the sensitivity of resistant AML cells to Ara-C. Resistant AML cells with or without stable NONO silencing were treated with Ara-C at a series of concentrations as indicated for 48 h, and cell viability was evaluated by a CCK-8 assay (n = 3, mean ± SD). C, D HL60-R (C) and HEL-R (D) cells with or without stably silencing NONO were transfected with SAMHD1 or Vector for 24 h. Then the cells were treated with Ara-C at the indicated concentrations for 48 h, and cell viability was evaluated by CCK-8 assay (n = 3, mean ± SD). E DDP and ADM sensitized resistant AML cells to Ara-C. Plots of the CIs for Ara-C and DDP or ADM in HL60-R and HEL-R cells, as determined using the Chou–Talalay method (n = 3). F NOD/SCID mice bearing HL60-R cell xenografts were treated with PBS, Ara-C, DDP, or a combination of Ara-C and DDP, and tumor growth was monitored. n = 6 for each group. G The tumor weights for each group as indicated in Fig. 7F. In B-D, 2-way ANOVA was used to compare the behavior of the cells treated as indicated and negative control cells. F, G, a two-tailed unpaired Student’s t test was used to determine statistical significance (**P < 0.01, ***P < 0.001). For respective immunoblots, the protein levels were quantified by ImageJ software.