Fig. 1

G0 leukemic cells induced by AraC or serum starvation are chemoresistant and recapitulate gene expression programs of in vivo chemoresistant and G0 models. a Ki67 translatome level and flow cytometric quantification of G0/G1, S, and G2/M phases, using BrdU and PI staining. Proliferating THP1 cells (S+ cells) were serum-starved for 4 days (SS cells) or treated with AraC for 3 days (AraCS cells). b Cell counting with trypan blue staining. THP1 cells were serum-starved or treated with AraC for days indicated. Then, serum was added to SS cells while AraCS cells were resuspended in fresh media. c S+, SS, and AraCS cells were treated with various concentration of AraC for 3 days. Viable THP1 leukemic cells were measured by cell counting using trypan blue staining and IC₅₀ values of AraC are shown. d Transcriptome, translatome, and proteome analyses in proliferating and G0 leukemic cells. G0 cells (AraCS, SS cells) were induced by treatment of proliferating cells (S+) with AraC or serum starvation. Total RNAs, polysome-associated mRNAs, and protein were analyzed by comparative microarray and quantitative proteomics. e Comparison of transcriptomic, translatomic, and proteomic changes in response to SS and 5 μM AraC treatments. f Comparison of AraCS and SS with leukemic stem cells (LSC) [16] in AML, dormant leukemic cells (LRC) [15], minimal residual disease (MRD) [15] in ALL, and G0 fibroblasts [1]. GSEA analysis was performed to determine whether previously published transcriptome signatures of LSC, LRC, MRD, and G0 HFF are upregulated in AraCS and SS cells, compared to S+ cells. “N” marks the limited resolution of the proteome in the GSEA. *p ≤ 0.05. Data are represented as average ± SEM. See also Additional file 1: Figure S1 and Additional file 2: Table S1