Supplementary Fig. S1-13 from M<sup>6</sup>A Demethylase ALKBH5 Regulates PD-L1 Expression and Tumor Immunoenvironment in Intrahepatic Cholangiocarcinoma

Supplementary Fig. S1. PD-L1 was regulated by ALKBH5 independent on FTO, METTL3 or METTL14. Supplementary Fig. S2. m6A-seq and mRNA-seq of RBE-shCtrl/shALKBH5 cells. Supplementary Fig. S3. Transient ALKBH5 and its mutant H204A overexpression increased the endogenous ALKBH5 protein level. Supplementary Fig. S4. ALKBH5 deficiency accelerates the degradation of PD-L1 mRNA dependent on YTHDF2. Supplementary Fig. S5. The role of YTHDF2 in regulating PD-L1 expression. Supplementary Fig. S6. Tumor cell intrinsic ALKBH5 facilitates tumor resistance to anti-tumor T cell immunity. Supplementary Fig. S7. T cell expansion was inhibited by tumor-intrinsic ALKBH5. Supplementary Fig. S8. The role of ALKBH5 in the proliferation and migration of ICC cell in vitro. Supplementary Fig. S9. PD-L1 is essential for ALKBH5-regulated anti-tumor T cell immunity. Supplementary Fig. S10. The correlation between ALKBH5 and PD-L1 transcripts in TCGA datasets. Supplementary Fig. S11. ALKBH5 positively correlates with PD-L1 expression in clinical ICC specimens. Supplementary Fig. S12. The role of ALKBH5 in ICC immune microenvironment. Supplementary Fig. S13. ALKBH5 deficiency in ICC cells relates to immunosuppressive microenvironment.