Table 1.
Effects and mechanisms of MSC-EXs on breast cancer.
| Source | Effect | Mechanism | Model | Ref |
|---|---|---|---|---|
| ADSC | Stimulating metastasis of BCC | Type 2 diabetes mellitus altered the functions of MSC-EVs | In vivo | [39] |
| ADSC | Reduced tumor cell proliferation and migration and enhanced tumor cell apoptosis | CD90 expression in different concentrations (CD90high ADSCs and CD90low ADSCs) on ADSC-EVs affected the antitumor activity | In vitro | [40] |
| BM-MSC | Suppressed the growth of triple-negative breast cancer | By secreting miR-106a-5p | In vivo | [41] |
| hUC-MSC | Promoted the invasion and migration potential of breast cancer cells | By activating the Akt pathway to promote epithelial-mesenchymal transition | In vitro | [36] |
| hMSC or mMSC | Promoted the progression of breast cancer | By inducing monocytic myeloid-derived suppressor cells to differentiate into highly immunosuppressed M2 polarized macrophages | In vivo | [42] |
MSC: mesenchymal stem cell; EV: extracellular vesicle; ADSC: adipose-derived MSC; BCC: breast cancer cell; MSC-EV: MSC-derived EV; ADSC-EV: ADSC-derived EV; BM-MSC: bone marrow MSC; hUC-MSC: human umbilical cord MSC; hMSC: human MSC; mMSC: mouse MSC.