Cancer-associated fibroblast-derived exosomal miR-18b promotes breast cancer invasion and metastasis by regulating TCEAL7

Abstract Studies have shown that cancer-associated fibroblasts (CAFs) play an irreplaceable role in the occurrence and development of tumors. Therefore, exploring the action and mechanism of CAFs on tumor cells is particularly important. In this study, we compared the effects of CAFs-derived exosome...

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Autores principales:	Ziqian Yan, Zhimei Sheng, Yuanhang Zheng, Ruijun Feng, Qinpei Xiao, Lihong Shi, Hongli Li, Chonggao Yin, Hao Luo, Chong Hao, Wenhao Wang, Baogang Zhang
Formato:	article
Lenguaje:	EN
Publicado:	Nature Publishing Group 2021
Materias:	Cytology QH573-671
Acceso en línea:	https://doaj.org/article/e8227a51e76e48daa6d2c4c58a484a5b
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spelling	oai:doaj.org-article:e8227a51e76e48daa6d2c4c58a484a5b2021-12-05T12:04:30ZCancer-associated fibroblast-derived exosomal miR-18b promotes breast cancer invasion and metastasis by regulating TCEAL710.1038/s41419-021-04409-w2041-4889https://doaj.org/article/e8227a51e76e48daa6d2c4c58a484a5b2021-12-01T00:00:00Zhttps://doi.org/10.1038/s41419-021-04409-whttps://doaj.org/toc/2041-4889Abstract Studies have shown that cancer-associated fibroblasts (CAFs) play an irreplaceable role in the occurrence and development of tumors. Therefore, exploring the action and mechanism of CAFs on tumor cells is particularly important. In this study, we compared the effects of CAFs-derived exosomes and normal fibroblasts (NFs)-derived exosomes on breast cancer cells migration and invasion. The results showed that exosomes from both CAFs and NFs could enter into breast cancer cells and CAFs-derived exosomes had a more enhancing effect on breast cancer cells migration and invasion than NFs-derived exosomes. Furthermore, microRNA (miR)-18b was upregulated in CAFs-derived exosomes, and CAFs-derived exosomes miR-18b can promote breast cancer cell migration and metastasis by specifically binding to the 3′UTR of Transcription Elongation Factor A Like 7 (TCEAL7). The miR-18b-TCEAL7 pathway promotes nuclear Snail ectopic activation by activating nuclear factor-kappa B (NF-κB), thereby inducing epithelial-mesenchymal transition (EMT) and promoting cell invasion and metastasis. Moreover, CAFs-derived exosomes miR-18b could promote mouse xenograft model tumor metastasis. Overall, our findings suggest that CAFs-derived exosomes miR-18b promote nuclear Snail ectopic by targeting TCEAL7 to activate the NF-κB pathway, thereby inducing EMT, invasion, and metastasis of breast cancer. Targeting CAFs-derived exosome miR-18b may be a potential treatment option to overcome breast cancer progression.Ziqian YanZhimei ShengYuanhang ZhengRuijun FengQinpei XiaoLihong ShiHongli LiChonggao YinHao LuoChong HaoWenhao WangBaogang ZhangNature Publishing GrouparticleCytologyQH573-671ENCell Death and Disease, Vol 12, Iss 12, Pp 1-14 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	Cytology QH573-671
spellingShingle	Cytology QH573-671 Ziqian Yan Zhimei Sheng Yuanhang Zheng Ruijun Feng Qinpei Xiao Lihong Shi Hongli Li Chonggao Yin Hao Luo Chong Hao Wenhao Wang Baogang Zhang Cancer-associated fibroblast-derived exosomal miR-18b promotes breast cancer invasion and metastasis by regulating TCEAL7
description	Abstract Studies have shown that cancer-associated fibroblasts (CAFs) play an irreplaceable role in the occurrence and development of tumors. Therefore, exploring the action and mechanism of CAFs on tumor cells is particularly important. In this study, we compared the effects of CAFs-derived exosomes and normal fibroblasts (NFs)-derived exosomes on breast cancer cells migration and invasion. The results showed that exosomes from both CAFs and NFs could enter into breast cancer cells and CAFs-derived exosomes had a more enhancing effect on breast cancer cells migration and invasion than NFs-derived exosomes. Furthermore, microRNA (miR)-18b was upregulated in CAFs-derived exosomes, and CAFs-derived exosomes miR-18b can promote breast cancer cell migration and metastasis by specifically binding to the 3′UTR of Transcription Elongation Factor A Like 7 (TCEAL7). The miR-18b-TCEAL7 pathway promotes nuclear Snail ectopic activation by activating nuclear factor-kappa B (NF-κB), thereby inducing epithelial-mesenchymal transition (EMT) and promoting cell invasion and metastasis. Moreover, CAFs-derived exosomes miR-18b could promote mouse xenograft model tumor metastasis. Overall, our findings suggest that CAFs-derived exosomes miR-18b promote nuclear Snail ectopic by targeting TCEAL7 to activate the NF-κB pathway, thereby inducing EMT, invasion, and metastasis of breast cancer. Targeting CAFs-derived exosome miR-18b may be a potential treatment option to overcome breast cancer progression.
format	article
author	Ziqian Yan Zhimei Sheng Yuanhang Zheng Ruijun Feng Qinpei Xiao Lihong Shi Hongli Li Chonggao Yin Hao Luo Chong Hao Wenhao Wang Baogang Zhang
author_facet	Ziqian Yan Zhimei Sheng Yuanhang Zheng Ruijun Feng Qinpei Xiao Lihong Shi Hongli Li Chonggao Yin Hao Luo Chong Hao Wenhao Wang Baogang Zhang
author_sort	Ziqian Yan
title	Cancer-associated fibroblast-derived exosomal miR-18b promotes breast cancer invasion and metastasis by regulating TCEAL7
title_short	Cancer-associated fibroblast-derived exosomal miR-18b promotes breast cancer invasion and metastasis by regulating TCEAL7
title_full	Cancer-associated fibroblast-derived exosomal miR-18b promotes breast cancer invasion and metastasis by regulating TCEAL7
title_fullStr	Cancer-associated fibroblast-derived exosomal miR-18b promotes breast cancer invasion and metastasis by regulating TCEAL7
title_full_unstemmed	Cancer-associated fibroblast-derived exosomal miR-18b promotes breast cancer invasion and metastasis by regulating TCEAL7
title_sort	cancer-associated fibroblast-derived exosomal mir-18b promotes breast cancer invasion and metastasis by regulating tceal7
publisher	Nature Publishing Group
publishDate	2021
url	https://doaj.org/article/e8227a51e76e48daa6d2c4c58a484a5b
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Cancer-associated fibroblast-derived exosomal miR-18b promotes breast cancer invasion and metastasis by regulating TCEAL7

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