Exosomes in ovarian cancer ascites promote epithelial–mesenchymal transition of ovarian cancer cells by delivery of miR-6780b-5p

Abstract The poor prognosis of ovarian cancer is mainly due to metastasis, and the specific mechanism underlying ovarian cancer metastasis is not clear. Ascites-derived exosomes (ADEs) play an important role in the progression of ovarian cancer, but the mechanism is unknown. Here, we found that ADEs...

Full description

Bibliographic Details
Main Authors: Jing Cai, Lanqing Gong, Guodong Li, Jing Guo, Xiaoqing Yi, Zehua Wang
Format: Article
Language:English
Published: Nature Publishing Group 2021-02-01
Series:Cell Death and Disease
Online Access:https://doi.org/10.1038/s41419-021-03490-5
id doaj-03918ed8f7534f8ea2fbd305388bbae9
record_format Article
spelling doaj-03918ed8f7534f8ea2fbd305388bbae92021-03-11T11:16:19ZengNature Publishing GroupCell Death and Disease2041-48892021-02-0112211710.1038/s41419-021-03490-5Exosomes in ovarian cancer ascites promote epithelial–mesenchymal transition of ovarian cancer cells by delivery of miR-6780b-5pJing Cai0Lanqing Gong1Guodong Li2Jing Guo3Xiaoqing Yi4Zehua Wang5Department of Obstetrics and Gynecology, Union Hospital, Tongji Medical College, Huazhong University of Science and TechnologyDepartment of Obstetrics and Gynecology, Union Hospital, Tongji Medical College, Huazhong University of Science and TechnologyCancer Research Institute, Tongji Hospital, Huazhong University of Science and TechnologyDepartment of Obstetrics and Gynecology, Union Hospital, Tongji Medical College, Huazhong University of Science and TechnologyDepartment of Obstetrics and Gynecology, Union Hospital, Tongji Medical College, Huazhong University of Science and TechnologyDepartment of Obstetrics and Gynecology, Union Hospital, Tongji Medical College, Huazhong University of Science and TechnologyAbstract The poor prognosis of ovarian cancer is mainly due to metastasis, and the specific mechanism underlying ovarian cancer metastasis is not clear. Ascites-derived exosomes (ADEs) play an important role in the progression of ovarian cancer, but the mechanism is unknown. Here, we found that ADEs promoted ovarian cancer metastasis not only in vitro but also in vivo. This promotive function was based on epithelial–mesenchymal transition (EMT) of ovarian cancer cells. Bioinformatics analysis of RNA sequencing microarray data indicated that miR-6780b-5p may be the key microRNA (miRNA) in ADEs that facilitates cancer metastasis. Moreover, the expression of exosomal miR-6780b-5p correlated with tumor metastasis in ovarian cancer patients. miR-6780b-5p overexpression promoted and miR-6780b-5p downregulation suppressed EMT of ovarian cancer cells. These results suggest that ADEs transfer miR-6780b-5p to ovarian cancer cells, promoting EMT and finally facilitating ovarian cancer metastasis.https://doi.org/10.1038/s41419-021-03490-5
collection DOAJ
language English
format Article
sources DOAJ
author Jing Cai
Lanqing Gong
Guodong Li
Jing Guo
Xiaoqing Yi
Zehua Wang
spellingShingle Jing Cai
Lanqing Gong
Guodong Li
Jing Guo
Xiaoqing Yi
Zehua Wang
Exosomes in ovarian cancer ascites promote epithelial–mesenchymal transition of ovarian cancer cells by delivery of miR-6780b-5p
Cell Death and Disease
author_facet Jing Cai
Lanqing Gong
Guodong Li
Jing Guo
Xiaoqing Yi
Zehua Wang
author_sort Jing Cai
title Exosomes in ovarian cancer ascites promote epithelial–mesenchymal transition of ovarian cancer cells by delivery of miR-6780b-5p
title_short Exosomes in ovarian cancer ascites promote epithelial–mesenchymal transition of ovarian cancer cells by delivery of miR-6780b-5p
title_full Exosomes in ovarian cancer ascites promote epithelial–mesenchymal transition of ovarian cancer cells by delivery of miR-6780b-5p
title_fullStr Exosomes in ovarian cancer ascites promote epithelial–mesenchymal transition of ovarian cancer cells by delivery of miR-6780b-5p
title_full_unstemmed Exosomes in ovarian cancer ascites promote epithelial–mesenchymal transition of ovarian cancer cells by delivery of miR-6780b-5p
title_sort exosomes in ovarian cancer ascites promote epithelial–mesenchymal transition of ovarian cancer cells by delivery of mir-6780b-5p
publisher Nature Publishing Group
series Cell Death and Disease
issn 2041-4889
publishDate 2021-02-01
description Abstract The poor prognosis of ovarian cancer is mainly due to metastasis, and the specific mechanism underlying ovarian cancer metastasis is not clear. Ascites-derived exosomes (ADEs) play an important role in the progression of ovarian cancer, but the mechanism is unknown. Here, we found that ADEs promoted ovarian cancer metastasis not only in vitro but also in vivo. This promotive function was based on epithelial–mesenchymal transition (EMT) of ovarian cancer cells. Bioinformatics analysis of RNA sequencing microarray data indicated that miR-6780b-5p may be the key microRNA (miRNA) in ADEs that facilitates cancer metastasis. Moreover, the expression of exosomal miR-6780b-5p correlated with tumor metastasis in ovarian cancer patients. miR-6780b-5p overexpression promoted and miR-6780b-5p downregulation suppressed EMT of ovarian cancer cells. These results suggest that ADEs transfer miR-6780b-5p to ovarian cancer cells, promoting EMT and finally facilitating ovarian cancer metastasis.
url https://doi.org/10.1038/s41419-021-03490-5
work_keys_str_mv AT jingcai exosomesinovariancancerascitespromoteepithelialmesenchymaltransitionofovariancancercellsbydeliveryofmir6780b5p
AT lanqinggong exosomesinovariancancerascitespromoteepithelialmesenchymaltransitionofovariancancercellsbydeliveryofmir6780b5p
AT guodongli exosomesinovariancancerascitespromoteepithelialmesenchymaltransitionofovariancancercellsbydeliveryofmir6780b5p
AT jingguo exosomesinovariancancerascitespromoteepithelialmesenchymaltransitionofovariancancercellsbydeliveryofmir6780b5p
AT xiaoqingyi exosomesinovariancancerascitespromoteepithelialmesenchymaltransitionofovariancancercellsbydeliveryofmir6780b5p
AT zehuawang exosomesinovariancancerascitespromoteepithelialmesenchymaltransitionofovariancancercellsbydeliveryofmir6780b5p
_version_ 1724225667146448896