Supplemental Table S1 | Primer sequences used in this study.;Supplemental Table S2 | List of 1639 TFs from Human Transcription Factors database.;Supplemental Table S3 | Potential STAT2 binding motifs on Region 1 and Region 2.;Supplemental Figures [Figure S1 (Identification of chromatin accessibilities using ATAC-seq profiles.), S2 (Integrative analysis identified STAT2 as a potential upstream for PD-L1.), and S3 (Validation of the interaction between STAT2 and PD-L1.)]

Supplemental Table S1 | Primer sequences used in this study.;Supplemental Table S2 | List of 1639 TFs from Human Transcription Factors database.;Supplemental Table S3 | Potential STAT2 binding motifs on Region 1 and Region 2.;Figure S1 | Identification of chromatin accessibilities using ATAC-seq profiles. (A)For the analysis of chromatin accessibilities, peak calling function was performed.The upset plot and vennpie plot revealed that a considerable fraction of open chromatin regions were around gene promoters. Figure S2 | Integrative analysis identified STAT2 as a potential upstream for PD-L1. (A) Correlation analysis between open chromatin regions and all the database-recorded TFs was performed. The TFs, which were correlated with Region 1 or Region 2, were displayed in the heatmap (r > 0.4, p < 0.05). Compared with other TFs, STAT2 was closely related with both Region 1 (left, r = 0.6, p < 0.05) and Region 2 (right, r = 0.5, p < 0.05). (B) Correlation analysis between PD-L1 expression and expression of the top 5 TFs associated with PD-L1 promoter region 1 or region 2 in Figure S2A. Of these top candidates, STAT2 was the TF with the strongest correlation with PD-L1 expression (r = 0.53, p < 0.05). Figure S3 | Validation of the interaction between STAT2 and PD-L1. (A) The analysis of protein-protein interactions, based on GeneMANIA database, indicated a potential interaction between STAT2 and PD-L1. (B) In cancer cell line HeLa, the overexpression of STAT2 could lead to upregulation of PD-L1 significantly (p < 0.05).