Fig. 8: Exosome-mediated transfer of miR-567 reverses trastuzumab resistance.

a Intercellular trafficking of exosomes among different cell lines by isolated exosomes labeled with PKH26 dye; scale bars: 10 μm. b Treatment with exosomes derived from MCF-10A cells increased miR-567 level; however, this increase was eliminated when MCF-10A cells were silenced with miR-567, *P < 0.05. c Western blotting showed that autophagy was induced in cells treated with MCF-10A-derived exosomes. d CCK8 assay showed that MCF-10A-derived exosomes induced chemosensitivity in SKBR-3-TR and BT474-TR cells, *P < 0.05. e Nano-sight particle tracking analysis of the size distributions and number of exosomes from SKBR-3-TR cells treated with nSMase, GW4869; **P < 0.01 compared with DMSO group. f CCK8 assay showed that incubation with exosomes from MCF-10A cells treated with GW4869 failed to reverse trastuzumab resistance to recipient cells. g CCK8 assay verified that silence of miR-567 inhibited the ability of co-cultured parental cells to acquire chemo-response. h A scheme of the proposed mechanisms. High expressed miR-567 in MCF-10A cells was secreted via packaging into exosomes. Then, the extracellular miR-567 was incorporated into recipient cells, suppressed autophagy, and reversed chemoresistance via suppressing ATG5 expression.