Table 2 Effect of exosome-derived miRNA released by tumor cells on CAFs

miR-500a-5p

CAFs promotes breast cancer progression and metastasis through exosome miR-500a-5p

By binding to ubiquitin-specific peptidase 28

[76]

miR-92

miR-92 secreted by CAFs significantly promotes tumor progression and impairs the function of tumor-infiltrating immune cells in vivo

LATS2 is thought to be a target gene for miR-92, and LATS2 interacts with YAP1

[79]

miR-185-5p,miR-652-5p,miR-1246

The synergistic effects of miR-185-5p, miR-652-5p, and miR-1246 promote fibroblast migration and contraction

Activate NFs to CAFs

[30]

miR-425-5p

R-425-5p promotes conversion to the CAFs phenotype and increases cell motility

By inhibiting its target gene TGFβRII

[80]

miR-222

MiR-222 overexpression or LBR knockdown is sufficient to induce NFs to exhibit CAFs signatures that enhance migration, invasion, and aging

Works by targeting LBR

[81]

miR-21, miR-143, miR-378

miRNAs exhibit significantly increased ability to form mammary globules, increased stem cells and EMT markers, and promote cell growth

Cell phenotypic changes

[82]

miR-146a

The miR-146a/TXNIP axis activates CAFs and activates the Wnt pathway, thereby promoting the invasion and metastasis of BC cells

Through the miR-146a/TXNIP axis, the wnt path is activated

[75]

miR-16, miR-148a

FAK ablation in CAFs increases the level of exosome miR-148a, thereby reducing the expression of WNT1 and WNT10B in recipient cancer cells

FAK signal transduction pathway

[83]

miR-330-5p

SNHG3 knockdown in CAF-secreted exosomes inhibits glycolytic metabolism by increasing miR-330-5p and decreasing PKM expression in tumor cells

Targeting lncRNA SNHG3

[84]

miR-1-3p

The elevation of miR-1-3p in breast cancer cells inhibits cell viability, invasion, migration and transformation from epithelium to mesenchymal, and inhibits tumor formation and metastasis

Targeting Gli-similar1 (GLIS1)

[85]