Anti-PD-L1 Antibody Enhances T Cell Immune Responses and Reduces Resistance of Breast Cancer Cells to Radiotherapy

Figure 3

miR-21 potentiates PD-L1 expression via activation of the PI3K/Akt pathway by targeting PDCD4 in BC cells. (a) Venn diagram depicting the intersection of target genes of miR-21 predicted with PicTar, miRDB, TargetScan, and starBase databases. (b) Protein-protein interaction network of the miR-21 downstream target genes. (c) Correlation between PDCD4 and miR-21 expression in BC tissue samples from the TCGA database. (d) Binding site between miR-21 and PDCD4 predicted using the TargetScan database. (e) The binding of miR-21 to PDCD4 confirmed by dual luciferase reporter gene assay. (f) Expression of miR-21, PDCD4, and PD-L1 after alteration of miR-21 and overexpression of PDCD4 determined by RT-qPCR in BC cells. compared with cells treated with mimic NC. ^# compared with cells treated with inhibitor NC and compared with cells treated with miR-21 mimic. (g) The silencing efficiency of si-PDCD4-1 and si-PDCD4-2 in BC cells determined by RT-qPCR. compared with cells treated with si-NC. (h) Western blot analysis of PDCD4, PI3K, Akt, and PD-L1 proteins, and the extent of PI3K and Akt phosphorylation in BC cells. compared with cells treated with oe-NC. ^# compared with cells treated with si-NC and compared with cells treated with si-PDCD4. Data () from two groups were compared using independent sample -test while those from multiple groups were compared using one-way ANOVA. All cell experiments were repeated 3 times independently.

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