Journal: Journal of Advanced Research

Article Title: Dynamic heterogeneity towards drug resistance in AML cells is primarily driven by epigenomic mechanism unveiled by multi-omics analysis

doi: 10.1016/j.jare.2025.05.038

Figure Lengend Snippet: Progressive dynamics of KG-1a post-Ara-C treatment. (A) Multiomics experimental design for KG-1a at different Ara-C treatment time points. (B) Sample source distribution. (C) RNA velocity analysis showing a continuous gene expression trajectory of KG-1a over different Ara-C treatment times. (D) CytoTRACE analysis indicating an increasing tread of developmental potential along Ara-C treatment time. The “stemness” degree of KG-1a cells reached a peak enduring 48-hour Ara-C treatment, and maintained a high level after acquiring the resistance. (E) The set of drug-resistant related genes expressed increasingly over Ara-C treatment times, and overall achieved the maximum of the expression in the resistant KG-1a cells.

Article Snippet: Chemotherapeutic agents Ara-C, DNR, AZA, and DEC were sourced from MedChemExpress (MCE, #HY-13605A; #HY-13062; #HY-10586; #HY-A0004).

Techniques: Gene Expression, Expressing

Journal: Journal of Advanced Research

Article Title: Dynamic heterogeneity towards drug resistance in AML cells is primarily driven by epigenomic mechanism unveiled by multi-omics analysis

doi: 10.1016/j.jare.2025.05.038

Figure Lengend Snippet: Identification of the cells potentially evading Ara-C treatment. (A) Clustering of KG-1a cells across six treatment time points. (B) In the naïve group, expression distribution of whole DEGs about the drug-resistant group. (C and D) G2/M and S phase distribution of all groups.

Article Snippet: Chemotherapeutic agents Ara-C, DNR, AZA, and DEC were sourced from MedChemExpress (MCE, #HY-13605A; #HY-13062; #HY-10586; #HY-A0004).

Techniques: Expressing

Journal: Journal of Advanced Research

Article Title: Dynamic heterogeneity towards drug resistance in AML cells is primarily driven by epigenomic mechanism unveiled by multi-omics analysis

doi: 10.1016/j.jare.2025.05.038

Figure Lengend Snippet: DNA methylation and WES characteristics of Ara-C resistant KG-1a. (A) Statistics of hypermethylated and hypomethylated sites in Ara-C resistant KG-1a compared to the naïve. (B) Statistics of hypermethylated and hypomethylated genes in Ara-C resistant KG-1a compared to the naïve. (C) Ara-C resistant KG-1a showing overall hypermethylation near TSS (upstream and downstream 5000 bp) compared to the naïve. (D) KEGG enrichment analysis of differential methylation sites of Ara-C resistant KG-1a versus naïve KG-1a. (E) Distribution of mutations detected in Ara-C resistant KG-1a compared to the naïve. (F) 20 genes with non-synonymous mutations detected in Ara-C resistant KG-1a compared to the naïve.

Article Snippet: Chemotherapeutic agents Ara-C, DNR, AZA, and DEC were sourced from MedChemExpress (MCE, #HY-13605A; #HY-13062; #HY-10586; #HY-A0004).

Techniques: DNA Methylation Assay, Methylation

Journal: Journal of Advanced Research

Article Title: Antimycin A inhibits alpha-herpesvirus replication by disrupting the formation of pyrimidinosomes

doi: 10.1016/j.jare.2025.05.016

Figure Lengend Snippet: Antiviral activity of Antimycin A in relevant cell lines and primary cells . Dose–response analysis of Antimycin A against the BHV-1 in MDBK cell line (A), plaque assay (B), Western blotting (C) and TCID 50 (D). MDBK cells were pretreated with increasing concentrations of Antimycin A or Ara-C (50 μM) for 12 h, followed by infection with BHV-1 wild type (WT) at an MOI of 0.5. (A) Dose–response analysis of Antimycin A against the BHV-1-ΔgIE-eGFP/Gluc, showing infectivity (black), cell number (orange) and IC50 values. (B) The quantity of released infectious virions was measured by plaque assay, with data representing the means ± SEM from n = 2 independent experiments, normalized to DMSO-treated controls. The anti-BHV-1 IC50 value was determined through nonlinear regression analysis. (C) Western blot analysis of infected cells after 24 h, using anti-BHV-1 serum to quantify infection levels, with β-actin as a loading control. (D) Quantified the released infectious virions by measuring the CPE in MDBK cells, and data are presented as log10 ± SEM of infectious particle concentration (TCID 50 /mL) from n = 3 independent experiments. HacaT cells (E), Vero-E6 cells (F), primary bovine turbinate osteocytes (G), and primary bovine tracheal epithelial cells (H) were pretreated for 12 h with various concentrations of Antimycin A and subsequently infected with BHV-1-ΔgIE-eGFP/Gluc at an MOI of 0.5. Infection levels were quantified 24 h later using a Gaussia Luciferase Flash Assay, while cell viability was measured using the CCK-8 Assay. (For interpretation of the references to colour in this figure legend, the reader is referred to the web version of this article.)

Article Snippet: The specific compounds used in this study included Antimycin A (MS0070-10MG; Maokang Biotechnology), Ara-C (MCE, HY-13605), Uridine (MCE, HY-B1449), Orotate (MCE, HY-N8060A), Dihydroorotate (MCE, HY-N0157), Aspartic Acid (MCE, HY-N0666R), Orotidine (MCE, 113226), Ascorbic Acid (MCE, B0166R), and BQR (MCE, 108325).

Techniques: Activity Assay, Plaque Assay, Western Blot, Infection, Control, Concentration Assay, Luciferase, CCK-8 Assay