Fig. 6
IL-6 promoted the expression of EIF4A3 in tumor cells via activating JAK2-STAT3 pathway. a Volcano plot showing differentially expressed genes in MCF-7 cells co-cultured with TAMOE−Exo compared to co-cultured with TAMEV−Exo. b GSEA showing significantly upregulated genes in MCF-7 cells co-cultured with TAMOE−Exo were significantly enrichment in JAK2-STAT3 pathway. c EIF4A3 expression in MCF-7 cells co-cultured with TAMEV−Exo or TAMOE−Exo was determined by qRT-PCR. d. Western blotting analysis (left) and quantification (right) of EIF4A3 level in MCF-7 cells co-cultured with TAMEV−Exo or TAMOE−Exo. e The relative expression of EIF4A3 in MCF-7 cells as indicated treatments. f Sequence motif representing the consensus STAT3 binding motif (JASPAR database, upper) and schematic diagram of the putative STAT3 binding site in the EIF4A3 promoter (lower). g ChIP assay was performed in MCF-7 cells co-cultured with TAMEV−Exo or TAMOE−Exo to detect the enrichment of potential binding sequences using the STAT3 antibody. h Luciferase reporter assay was performed to validate the interaction between STAT3 and the two binding sites (BS1 and BS2). i Schematic illustrating the molecular mechanism of tumor exosomal cSERPINE2 triggered a positive feedback loop between tumor cells and TAMs to promote breast cancer progression. Data are presented as the means ± SD of three independent experiments. *P < 0.05, **P < 0.01, ***P < 0.001