AUTHOR=Zhu Yanbo , Li Fang , Wan Yilong , Liang Hansi , Li Si , Peng Bo , Shao Liqun , Xu Yunyun , Jiang Dong 

TITLE=Cancer-Secreted Exosomal MiR-620 Inhibits ESCC Aerobic Glycolysis via FOXM1/HER2 Pathway and Promotes Metastasis

JOURNAL=Frontiers in Oncology

VOLUME=12

YEAR=2022

URL=https://www.frontiersin.org/journals/oncology/articles/10.3389/fonc.2022.756109

DOI=10.3389/fonc.2022.756109

ISSN=2234-943X

ABSTRACT=<sec><title>Background</title><p>Esophageal squamous cell carcinoma (ESCC) is a leading cause of cancer death worldwide. MicroRNAs (MiRNAs) have been reported to regulate cell functions through exosomes. Through the Gene Expression Omnibus (GEO) database, miR-620 was selected as a serum miRNA highly expressed in ESCC, but its detailed role in ESCC has not been explored. Tumor-secreted miRNAs have been reported to promote cancer metastasis through reprogramming the aerobic glycolysis of lung fibroblasts. Therefore, we intended to verify whether exosomal miR-620 secreted in ESCC cells may regulate the aerobic glycolysis of lung fibroblasts.</p></sec><sec><title>Methods</title><p>The effect of miR-620 on the aerobic glycolysis of ESCC cells was firstly verified through bioinformatics prediction and mechanism assays. Exosomes secreted from ESCC cells was detected, and the influence of exosomal miR-620 in regulating the aerobic glycolysis of lung fibroblasts was then verified both <italic>in vitro</italic> and <italic>in vivo</italic>.</p></sec><sec><title>Results</title><p>MiR-620 inhibited ESCC malignancy and suppressed the aerobic glycolysis of ESCC cells <italic>via</italic> targeting Forkhead box M1 (FOXM1) and human epidermal growth factor receptor 2 (HER2). Moreover, exosomal miR-620 was highly secreted in ESCC and could regulate HFL1 aerobic glycolysis <italic>via</italic> FOXM1/HER2 signaling. Furthermore, exosomal miR-620 could promote ESCC metastasis by reprogramming the aerobic glycolysis of lung fibroblasts (HFL1).</p></sec><sec><title>Conclusion</title><p>Exosomal miR-620 secreted by ESCC cells inhibited the aerobic glycolysis <italic>via</italic> FOXM1/HER2 axis and promoted cancer metastasis.</p></sec>