Bone marrow mesenchymal stem cells-derived exosomal microRNA-16-5p restrains epithelial-mesenchymal transition in breast cancer cells via EPHA1/NF-κB signaling axis

Objective: This study intends to conquer the mystery of microRNA-16-5p/erythropoietin-producing hepatocel-lular A1/nuclear factor-kappa B signaling (miR-16-5p/EPHA1/NF-kappa B signaling) in breast cancer. Methods: Expression of miR-16-5p, EPHA1 and NF-kappa B signaling-related proteins were detected. Gene over-expression or silencing was used to examine the biological roles of bone marrow mesenchymal stem cells (BMSCs)-derived exo-miR-16-5p in breast cancer. The effect of exo-miR-16-5p on tumorigenesis of breast cancer was confirmed by the xenograft nude mouse model. Results: Low miR-16-5p and high EPHA1 expression were examined in breast cancer. BMSCs-derived exosomes, up-regulated miR-16-5p or down-regulated EPHA1 restrained epithelial-mesenchymal transition (EMT) of breast cancer cells and tumor growth in nude mice. Down-regulated miR-16-5p or up-regulated EPHA1 activated NF-kappa B signaling. Knockdown of EPHA1 or inhibition of NF-kappa B signaling reversed the effects of down-regulated miR-16-5p on breast cancer cells. Conclusion: BMSCs-derived exosomal miR-16-5p hinders breast cancer cells progression via EPHA1/NF-kappa B signaling axis.

Automated summary

This study revealed that BMSCs-derived exosomal miR-16-5p can inhibit the growth and metastasis of breast cancer cells through modulation of the EPHA1/NF-kappa B signaling pathway.