miR-539 activates the SAPK/JNK signaling pathway to promote ferropotosis in colorectal cancer by directly targeting TIPE

Colorectal cancer (CRC) is a common tumor that harms human health with a high recurrence rate. It has been reported that the expression of microRNA-539 (miR-539) is low in several types of cancer, including CRC. Tumor necrosis factor (TNF)-α-induced protein 8 (TNFAIP8/TIPE) is highly expressed in CR...

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Autores principales: Yang, Yan, Lin, Zeyang, Han, Zhaopu, Wu, Zhengxin, Hua, Jianyu, Zhong, Rui, Zhao, Ruidan, Ran, Honggang, Qu, Kaiyong, Huang, Hongfei, Tang, Huamei, Huang, Jiyi, Liu, Zhongchen, Hong, Xuehui, Peng, Zhihai, Zhuang, Guohong
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group UK 2021
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Article
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8487425/
https://www.ncbi.nlm.nih.gov/pubmed/34601499
http://dx.doi.org/10.1038/s41420-021-00659-x
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author Yang, Yan
Lin, Zeyang
Han, Zhaopu
Wu, Zhengxin
Hua, Jianyu
Zhong, Rui
Zhao, Ruidan
Ran, Honggang
Qu, Kaiyong
Huang, Hongfei
Tang, Huamei
Huang, Jiyi
Liu, Zhongchen
Hong, Xuehui
Peng, Zhihai
Zhuang, Guohong
author_facet Yang, Yan
Lin, Zeyang
Han, Zhaopu
Wu, Zhengxin
Hua, Jianyu
Zhong, Rui
Zhao, Ruidan
Ran, Honggang
Qu, Kaiyong
Huang, Hongfei
Tang, Huamei
Huang, Jiyi
Liu, Zhongchen
Hong, Xuehui
Peng, Zhihai
Zhuang, Guohong
author_sort Yang, Yan
collection PubMed
description Colorectal cancer (CRC) is a common tumor that harms human health with a high recurrence rate. It has been reported that the expression of microRNA-539 (miR-539) is low in several types of cancer, including CRC. Tumor necrosis factor (TNF)-α-induced protein 8 (TNFAIP8/TIPE) is highly expressed in CRC and promotes the proliferation, migration and angiogenesis of CRC. However, the relationship between miR-539 and TIPE and the mechanisms by which they regulate the proliferation of CRC remain to be explored. We aimed to investigate the functions and mechanisms of miR-539 in CRC proliferation. Functionally, miR-539 can bind to and regulate the expression of TIPE, and miR-539 activates SAPK/JNK to downregulate the expression of glutathione peroxidase 4 (GPX4) and promote ferroptosis. Our data reveal the novel role of miR-539 in regulating ferroptosis in CRC via activation of the SAPK/JNK axis, providing new insight into the mechanism of abnormal proliferation in CRC and a novel potential therapeutic target for advanced CRC.
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spelling pubmed-84874252021-10-07 miR-539 activates the SAPK/JNK signaling pathway to promote ferropotosis in colorectal cancer by directly targeting TIPE Yang, Yan Lin, Zeyang Han, Zhaopu Wu, Zhengxin Hua, Jianyu Zhong, Rui Zhao, Ruidan Ran, Honggang Qu, Kaiyong Huang, Hongfei Tang, Huamei Huang, Jiyi Liu, Zhongchen Hong, Xuehui Peng, Zhihai Zhuang, Guohong Cell Death Discov Article Colorectal cancer (CRC) is a common tumor that harms human health with a high recurrence rate. It has been reported that the expression of microRNA-539 (miR-539) is low in several types of cancer, including CRC. Tumor necrosis factor (TNF)-α-induced protein 8 (TNFAIP8/TIPE) is highly expressed in CRC and promotes the proliferation, migration and angiogenesis of CRC. However, the relationship between miR-539 and TIPE and the mechanisms by which they regulate the proliferation of CRC remain to be explored. We aimed to investigate the functions and mechanisms of miR-539 in CRC proliferation. Functionally, miR-539 can bind to and regulate the expression of TIPE, and miR-539 activates SAPK/JNK to downregulate the expression of glutathione peroxidase 4 (GPX4) and promote ferroptosis. Our data reveal the novel role of miR-539 in regulating ferroptosis in CRC via activation of the SAPK/JNK axis, providing new insight into the mechanism of abnormal proliferation in CRC and a novel potential therapeutic target for advanced CRC. Nature Publishing Group UK 2021-10-02 /pmc/articles/PMC8487425/ /pubmed/34601499 http://dx.doi.org/10.1038/s41420-021-00659-x Text en © The Author(s) 2021 https://creativecommons.org/licenses/by/4.0/Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) .
spellingShingle Article
Yang, Yan
Lin, Zeyang
Han, Zhaopu
Wu, Zhengxin
Hua, Jianyu
Zhong, Rui
Zhao, Ruidan
Ran, Honggang
Qu, Kaiyong
Huang, Hongfei
Tang, Huamei
Huang, Jiyi
Liu, Zhongchen
Hong, Xuehui
Peng, Zhihai
Zhuang, Guohong
miR-539 activates the SAPK/JNK signaling pathway to promote ferropotosis in colorectal cancer by directly targeting TIPE
title miR-539 activates the SAPK/JNK signaling pathway to promote ferropotosis in colorectal cancer by directly targeting TIPE
title_full miR-539 activates the SAPK/JNK signaling pathway to promote ferropotosis in colorectal cancer by directly targeting TIPE
title_fullStr miR-539 activates the SAPK/JNK signaling pathway to promote ferropotosis in colorectal cancer by directly targeting TIPE
title_full_unstemmed miR-539 activates the SAPK/JNK signaling pathway to promote ferropotosis in colorectal cancer by directly targeting TIPE
title_short miR-539 activates the SAPK/JNK signaling pathway to promote ferropotosis in colorectal cancer by directly targeting TIPE
title_sort mir-539 activates the sapk/jnk signaling pathway to promote ferropotosis in colorectal cancer by directly targeting tipe
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8487425/
https://www.ncbi.nlm.nih.gov/pubmed/34601499
http://dx.doi.org/10.1038/s41420-021-00659-x
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