Additional file 1 of Epigenetic priming improves salvage chemotherapy in diffuse large B-cell lymphoma via endogenous retrovirus-induced cGAS-STING activation
Creators: name: Liu, Jun
name: Min, Suji
name: Kim, Dongchan
name: Park, Jihyun
name: Park, Eunchae
name: Koh, Youngil
name: Shin, Dong-Yeop
name: Kim, Tae Kon
name: Byun, Ja Min
name: Yoon, Sung-Soo
name: Hong, Junshik
Publisher: name: figshare
Year: 2024
Subjects: subject: Cell Biology
subject: Pharmacology
subject: Biotechnology
subject: Immunology
subject: FOS: Clinical medicine
subject: Biological Sciences not elsewhere classified
subject: Cancer
subject: Hematology

description: Additional file 1: Figure S1. A-B. Schematics of the in vitro and in vivo treatment regimens, respectively. Figure S2. A-F. Six DLBCL cell lines were exposed to 5-azacytidine (0.3 µM) or PBS for three consecutive days followed by treatment with different doses of cisplatin for 48 hours. Cell viability measured on day 5 (normalized to that on day 3 for AZA- or PBS-treated cells) is shown. Figure S3. A, Gene expression profiles between the cisplatin-sensitive group and cisplatin-resistant group are shown using a heatmap. R: Resistant, S: Sensitive, RS: Re-sensitization. B, Gene expression profiles without or with 5-azacytidine treatment are shown using a heatmap. Figure S4. The expression level of ADAR1 determined using western blotting and RNAseq-based normalized expression data. Figure S5. Cell viability assay, OCI-LY1, SU-DHL2 and SU-DHL8 cells were treated with PBS, AZA, RTi, and AZA+RTi, followed by treatment with different doses of cisplatin for 48 hours. AZA: 5-azacytidine, RTi: reverse transcriptase inhibitor (delavirdine mesylate). Figure S6. The LINEs expression levels in each cell lines treated with PBS or 5-azacytidine were shown using a bar chat. Figure S7. A-B. OCI-LY1 and SU-DHL2 cells were treated with 0.3 µM 5-azacytidine for three consecutive days and 250 µM vitamin C once exposed for three days or only 0.3 µM 5-azacytidine or PBS for three consecutive days, followed by treatment with different doses of cisplatin for 48 hours. C-E, Subcutaneous tumor sizes, xenograft tumor images and tumor weights of xenografts from OCI-LY1 tumor-bearing models are shown. *p &lt; 0.05, *p &lt; 0.01 and ***p &lt; 0.001 two-way ANOVA). F. The expression level of TET2 determined using RNAseq-based normalized expression data is shown in a heatmap. Figure S8. Schematic diagram showed the background of the current study. Epigenetic priming-induced chemosensitization is a potential solution for the unmet needs of salvage chemotherapy, however, its potential and mechanism to improve outcomes in relapsed/refractory DLBCL is unknow. Figure S9. (A-B) MB21D1 and TMEM173, encoded cGAS and STING respectively, normalized expression level in 37 DLBCL patients (TCGA, PanCancer Atlas), (C) Concept schematic diagram to stratify DLBCL patients according to cGAS/STING expression level. The dots represent TCGA DLBCL patients’ cGAS and STING expression levels. Figure S10. Vitamin C showed the potential to improve insufficient epigenetic priming, and this effect was dependent on the GLUT3 level. Table S1. Antibodies. Table S2. RT–qPCR primer sequences. Table S3. siRNA sequences.