Bone Marrow Mesenchymal Stem Cell-Derived Exosomal miR-126 Inhibits Colon Cancer by Targeting PLEXIN-B2

Author:

Liu Zongfeng1,Jia Yuanji1,Guo Lijun2,Feng Meng1,Qi Ying1,Wang Shukun1,Sun Chenglin1

Affiliation:

1. Department of General Surgery, Central Hospital Affiliated to Shenyang Medical College, Shenyang, 110021, China

2. Inner Mongolia Forestry General Hospital, Inner Mongolia, 022150, China

Abstract

Recent studies demonstrated that bone mesenchymal stem cells (BMSCs) can be recruited to the tumor microenvironment, and exosomes secreted by BMSCs have new function in the intercellular communication of human cancer. To explore the effects of human BMSCs-derived exosomal miR-126 on the proliferation, migration and invasion of colon cancer. BMSCs were transfected with mimic and inhibitor of miR-126, respectively. Then after BMSCs treated with mimic or inhibitor, we isolated exosomes from BMSCs. The viability, migration and invasion ability of Colon cells were detected via methyl thiazolyl tetrazolium (MTT) assay and Transwell assay, respectively. The targeting relation between miR-126 and plexin-B2 (PLXNB2) was verified by using bioinformatics analysis and dual luciferase reporter assay. The expressions of PLXNB2 and related proteins in Colon cells were determined by Western blot. miR-126 expressed higher in exosomes from BMSCs, compared with control group. Moreover, overexpression of miR-126 inhibited cell viability, migration and invasion. In addition, Exosomal miR-126 lead to targeted inhibition of PLXNB2 in Colon cells. What’s more, according to the analysis of exosome content, miR-126 could mediate the inhibitory effect of exosomes on HCT116 and SW620 cells via negative regulating of PLXNB2. The results of our study showed that BMSCs-derived exosomal miR-126 could inhibit cell viability, cell migration and cell invasion.

Publisher

American Scientific Publishers

Subject

Pharmaceutical Science,General Materials Science,Biomedical Engineering,Medicine (miscellaneous),Bioengineering

Reference62 articles.

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