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Fig. 1 | Journal of Nanobiotechnology

Fig. 1

From: Intervening in hnRNPA2B1-mediated exosomal transfer of tumor-suppressive miR-184-3p for tumor microenvironment regulation and cancer therapy

Fig. 1

T-exo promoted tumor progression by inducing M2 macrophage polarization, which was blocked by Ex 26-CSOPOSA/JQ1. FCM for CD206 levels (a) and ELISA for the secretion of IL-10 (b) of T-exo-stimulated macrophages with or without the pretreatment of JQ1 or Ex 26-CSOPOSA/JQ1 (n = 3). c The proliferation of 4T1 cells cultured with MCM from macrophages treated as described above assessed by MTT assay (n = 3). Representative images of transwell migration assay (d) and the relative migration cell number (e) of 4T1 cells co-cultured with M0 macrophages (4T1-co-M0) treated as described above (n = 3). Tumor volume changes (f), image of tumors (g) and tumor weight (h) of each group (n = 5). i The expression of Cd206 in tumor tissues detected by qRT-PCR (n = 3). The fluorescence intensity of PKH67 measured by FCM (j) and fluorescence spectrophotometry (k) in macrophages after incubated with PKH67-labelled T-exo with or without the pretreatment of JQ1 or Ex 26-CSOPOSA/JQ1 (n = 3). The uptake mechanism of PKH67-labelled T-exo by macrophages tested by FCM (l) and fluorescence spectrophotometry (m) by pretreating cells with inhibitors of different internalization pathways. n The levels of Rac1 in macrophages determined by IF staining. Cell nuclei were blue. Rac1 was red. o MFI of Rac1 in (n) calculated by ImageJ software (n = 3). Data were expressed as mean ± SD (*p < 0.05, **p < 0.01, ***p < 0.001)

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