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

Abstract

OBJECTIVE:

This study intends to conquer the mystery of microRNA-16-5p/erythropoietin-producing hepatocellular A1/nuclear factor-κB signaling (miR-16-5p/EPHA1/NF-κB signaling) in breast cancer.

METHODS:

Expression of miR-16-5p, EPHA1 and NF-κB signaling-related proteins were detected. Gene overexpression 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-κB signaling. Knockdown of EPHA1 or inhibition of NF-κB 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-κB signaling axis.

• Authors: Yuan Zhang, Xiaofeng Lai, Qingfang Yue, Fei Cao, Yue Zhang, Yang Sun, Jun Tian, Yizhao Lu, Li He, Jun Bai, Yifang Wei
• Journal: Genomics (Genomics) Vol. 114 Issue 3 Pg. 110341 (05 2022) ISSN: 1089-8646 [Electronic] United States
• PMID: 35283197 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
• Copyright: Copyright © 2022. Published by Elsevier Inc.

Chemical References

• MicroRNAs
• MIRN16 microRNA, human
• Mirn16 microRNA, mouse
• NF-kappa B
• Receptor, EphA1

Topics

• Animals
• Humans
• Mice
• Disease Models, Animal
• Epithelial-Mesenchymal Transition
• Mesenchymal Stem Cells (metabolism)
• Mice, Nude
• MicroRNAs (genetics, metabolism)
• Neoplasms (metabolism)
• NF-kappa B (metabolism)
• Receptor, EphA1 (metabolism)