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癌症分泌的外泌体miR-620抑制食管鳞癌有氧糖酵解的FOXM1/HER2途径并促进转移。

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

作者信息

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

机构信息

Department of Oncology, First Affiliated Hospital of Soochow University, Suzhou, China.

Department of Human Anatomy and Histology & Embryology, The School of Biology & Basic Medical Sciences, Soochow University, Suzhou, China.

出版信息

Front Oncol. 2022 May 16;12:756109. doi: 10.3389/fonc.2022.756109. eCollection 2022.

DOI:10.3389/fonc.2022.756109
PMID:35651785
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9148961/
Abstract

BACKGROUND

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.

METHODS

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 and .

RESULTS

MiR-620 inhibited ESCC malignancy and suppressed the aerobic glycolysis of ESCC cells 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 FOXM1/HER2 signaling. Furthermore, exosomal miR-620 could promote ESCC metastasis by reprogramming the aerobic glycolysis of lung fibroblasts (HFL1).

CONCLUSION

Exosomal miR-620 secreted by ESCC cells inhibited the aerobic glycolysis FOXM1/HER2 axis and promoted cancer metastasis.

摘要

背景

食管鳞状细胞癌（ESCC）是全球癌症死亡的主要原因。据报道，微小RNA（miRNA）可通过外泌体调节细胞功能。通过基因表达综合数据库（GEO），miR-620被选为在ESCC中高表达的血清miRNA，但其在ESCC中的具体作用尚未得到探索。据报道，肿瘤分泌的miRNA可通过重编程肺成纤维细胞的有氧糖酵解促进癌症转移。因此，我们旨在验证ESCC细胞分泌的外泌体miR-620是否可能调节肺成纤维细胞的有氧糖酵解。

方法

首先通过生物信息学预测和机制分析验证miR-620对ESCC细胞有氧糖酵解的影响。检测ESCC细胞分泌的外泌体，然后在体内和体外验证外泌体miR-620在调节肺成纤维细胞有氧糖酵解中的作用。

结果

miR-620通过靶向叉头框M1（FOXM1）和人表皮生长因子受体2（HER2）抑制ESCC恶性肿瘤并抑制ESCC细胞的有氧糖酵解。此外，外泌体miR-620在ESCC中高分泌，并可通过FOXM1/HER2信号通路调节HFL1有氧糖酵解。此外，外泌体miR-620可通过重编程肺成纤维细胞（HFL1）的有氧糖酵解促进ESCC转移。

结论

ESCC细胞分泌的外泌体miR-620通过FOXM1/HER2轴抑制有氧糖酵解并促进癌症转移。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/746b/9148961/dc929ed8dca2/fonc-12-756109-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/746b/9148961/8d7b2f96a0d1/fonc-12-756109-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/746b/9148961/3d7afa90bcd3/fonc-12-756109-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/746b/9148961/942d29e15dcf/fonc-12-756109-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/746b/9148961/ddaf4697d778/fonc-12-756109-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/746b/9148961/fa305abf6094/fonc-12-756109-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/746b/9148961/fc19bea08e85/fonc-12-756109-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/746b/9148961/5c09e9e0c642/fonc-12-756109-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/746b/9148961/dc929ed8dca2/fonc-12-756109-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/746b/9148961/8d7b2f96a0d1/fonc-12-756109-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/746b/9148961/3d7afa90bcd3/fonc-12-756109-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/746b/9148961/942d29e15dcf/fonc-12-756109-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/746b/9148961/ddaf4697d778/fonc-12-756109-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/746b/9148961/fa305abf6094/fonc-12-756109-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/746b/9148961/fc19bea08e85/fonc-12-756109-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/746b/9148961/5c09e9e0c642/fonc-12-756109-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/746b/9148961/dc929ed8dca2/fonc-12-756109-g008.jpg

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