β-Arrestin1 Promotes Colorectal Cancer Metastasis Through GSK-3β/β-Catenin Signaling- Mediated Epithelial-to-Mesenchymal Transition
Recurrence and metastasis seriously affects the prognosis of patients with tumors, and the epithelial-to-mesenchymal transition (EMT) plays a key role in promoting tumor invasion and metastasis. Previous studies have showed that β-arrestin1 acted as a tumor-promoting factor in multiple types of tumo...
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Frontiers Media S.A.
2021-04-01
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Online Access: | https://www.frontiersin.org/articles/10.3389/fcell.2021.650067/full |
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author | Qing Song Qing Song Qing Song Zhifen Han Zhifen Han Xinnan Wu Xinnan Wu Yan Wang Yan Wang Lihong Zhou Lihong Zhou Liu Yang Liu Yang Ningning Liu Ningning Liu Hua Sui Hua Sui Jianfeng Cai Qing Ji Qing Ji Qi Li Qi Li |
author_facet | Qing Song Qing Song Qing Song Zhifen Han Zhifen Han Xinnan Wu Xinnan Wu Yan Wang Yan Wang Lihong Zhou Lihong Zhou Liu Yang Liu Yang Ningning Liu Ningning Liu Hua Sui Hua Sui Jianfeng Cai Qing Ji Qing Ji Qi Li Qi Li |
author_sort | Qing Song |
collection | DOAJ |
description | Recurrence and metastasis seriously affects the prognosis of patients with tumors, and the epithelial-to-mesenchymal transition (EMT) plays a key role in promoting tumor invasion and metastasis. Previous studies have showed that β-arrestin1 acted as a tumor-promoting factor in multiple types of tumor. However, the exact role and mechanism of β-arrestin1 in colorectal cancer (CRC) progression remains to be elucidated. Our research aimed to explore the potential mechanism underlying the role of β-arrestin1 in CRC metastasis. The expression of β-arrestin1 was investigated in both primary and metastatic CRC tissues using the GSE41258 database, and it was revealed that CRC patients with liver/lung metastasis had a higher expression level of β-arrestin1, and the expression level of β-arrestin1 was inversely correlated with the prognosis of CRC patients. Further in vitro mechanism studies indicated that β-arrestin1 had the ability to promote the migration of CRC cells through regulating the EMT process by activating Wingless/integration-1 (Wnt)/β-catenin signaling pathways. Blocking Wnt/β-catenin signaling with inhibitor ICG001 decreased the promoting effect of β-arrestin1 on EMT in CRC. In vivo imaging experiments further demonstrated the promoting effect of β-arrestin1 on the lung metastasis of CRC cells by tail vein injection in mice. The results of this paper suggest that β-arrestin1 promotes EMT via Wnt/β-catenin signaling pathway in CRC metastasis, and provides a novel therapeutic target for CRC metastasis. |
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language | English |
last_indexed | 2024-12-14T00:58:39Z |
publishDate | 2021-04-01 |
publisher | Frontiers Media S.A. |
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series | Frontiers in Cell and Developmental Biology |
spelling | doaj.art-dbf98965b54844bb8a408f8a0c03c79e2022-12-21T23:23:24ZengFrontiers Media S.A.Frontiers in Cell and Developmental Biology2296-634X2021-04-01910.3389/fcell.2021.650067650067β-Arrestin1 Promotes Colorectal Cancer Metastasis Through GSK-3β/β-Catenin Signaling- Mediated Epithelial-to-Mesenchymal TransitionQing Song0Qing Song1Qing Song2Zhifen Han3Zhifen Han4Xinnan Wu5Xinnan Wu6Yan Wang7Yan Wang8Lihong Zhou9Lihong Zhou10Liu Yang11Liu Yang12Ningning Liu13Ningning Liu14Hua Sui15Hua Sui16Jianfeng Cai17Qing Ji18Qing Ji19Qi Li20Qi Li21Department of Medical Oncology and Cancer Institute of Integrative Medicine, Shuguang Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai, ChinaAcademy of Integrative Medicine, Shanghai University of Traditional Chinese Medicine, Shanghai, ChinaDepartment of Medical Oncology, Suzhou TCM Hospital Affiliated to Nanjing University of Chinese Medicine, Suzhou, ChinaDepartment of Medical Oncology and Cancer Institute of Integrative Medicine, Shuguang Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai, ChinaAcademy of Integrative Medicine, Shanghai University of Traditional Chinese Medicine, Shanghai, ChinaDepartment of Medical Oncology and Cancer Institute of Integrative Medicine, Shuguang Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai, ChinaAcademy of Integrative Medicine, Shanghai University of Traditional Chinese Medicine, Shanghai, ChinaDepartment of Medical Oncology and Cancer Institute of Integrative Medicine, Shuguang Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai, ChinaAcademy of Integrative Medicine, Shanghai University of Traditional Chinese Medicine, Shanghai, ChinaDepartment of Medical Oncology and Cancer Institute of Integrative Medicine, Shuguang Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai, ChinaAcademy of Integrative Medicine, Shanghai University of Traditional Chinese Medicine, Shanghai, ChinaDepartment of Medical Oncology and Cancer Institute of Integrative Medicine, Shuguang Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai, ChinaAcademy of Integrative Medicine, Shanghai University of Traditional Chinese Medicine, Shanghai, ChinaDepartment of Medical Oncology and Cancer Institute of Integrative Medicine, Shuguang Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai, ChinaAcademy of Integrative Medicine, Shanghai University of Traditional Chinese Medicine, Shanghai, ChinaDepartment of Medical Oncology and Cancer Institute of Integrative Medicine, Shuguang Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai, ChinaAcademy of Integrative Medicine, Shanghai University of Traditional Chinese Medicine, Shanghai, ChinaDepartment of Chemistry, University of South Florida, Tampa, FL, United StatesDepartment of Medical Oncology and Cancer Institute of Integrative Medicine, Shuguang Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai, ChinaAcademy of Integrative Medicine, Shanghai University of Traditional Chinese Medicine, Shanghai, ChinaDepartment of Medical Oncology and Cancer Institute of Integrative Medicine, Shuguang Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai, ChinaAcademy of Integrative Medicine, Shanghai University of Traditional Chinese Medicine, Shanghai, ChinaRecurrence and metastasis seriously affects the prognosis of patients with tumors, and the epithelial-to-mesenchymal transition (EMT) plays a key role in promoting tumor invasion and metastasis. Previous studies have showed that β-arrestin1 acted as a tumor-promoting factor in multiple types of tumor. However, the exact role and mechanism of β-arrestin1 in colorectal cancer (CRC) progression remains to be elucidated. Our research aimed to explore the potential mechanism underlying the role of β-arrestin1 in CRC metastasis. The expression of β-arrestin1 was investigated in both primary and metastatic CRC tissues using the GSE41258 database, and it was revealed that CRC patients with liver/lung metastasis had a higher expression level of β-arrestin1, and the expression level of β-arrestin1 was inversely correlated with the prognosis of CRC patients. Further in vitro mechanism studies indicated that β-arrestin1 had the ability to promote the migration of CRC cells through regulating the EMT process by activating Wingless/integration-1 (Wnt)/β-catenin signaling pathways. Blocking Wnt/β-catenin signaling with inhibitor ICG001 decreased the promoting effect of β-arrestin1 on EMT in CRC. In vivo imaging experiments further demonstrated the promoting effect of β-arrestin1 on the lung metastasis of CRC cells by tail vein injection in mice. The results of this paper suggest that β-arrestin1 promotes EMT via Wnt/β-catenin signaling pathway in CRC metastasis, and provides a novel therapeutic target for CRC metastasis.https://www.frontiersin.org/articles/10.3389/fcell.2021.650067/fullcolorectal cancerepithelial-to-mesenchymal transitionmetastasisβ-arrestin1Wnt/β-catenin signaling pathway |
spellingShingle | Qing Song Qing Song Qing Song Zhifen Han Zhifen Han Xinnan Wu Xinnan Wu Yan Wang Yan Wang Lihong Zhou Lihong Zhou Liu Yang Liu Yang Ningning Liu Ningning Liu Hua Sui Hua Sui Jianfeng Cai Qing Ji Qing Ji Qi Li Qi Li β-Arrestin1 Promotes Colorectal Cancer Metastasis Through GSK-3β/β-Catenin Signaling- Mediated Epithelial-to-Mesenchymal Transition Frontiers in Cell and Developmental Biology colorectal cancer epithelial-to-mesenchymal transition metastasis β-arrestin1 Wnt/β-catenin signaling pathway |
title | β-Arrestin1 Promotes Colorectal Cancer Metastasis Through GSK-3β/β-Catenin Signaling- Mediated Epithelial-to-Mesenchymal Transition |
title_full | β-Arrestin1 Promotes Colorectal Cancer Metastasis Through GSK-3β/β-Catenin Signaling- Mediated Epithelial-to-Mesenchymal Transition |
title_fullStr | β-Arrestin1 Promotes Colorectal Cancer Metastasis Through GSK-3β/β-Catenin Signaling- Mediated Epithelial-to-Mesenchymal Transition |
title_full_unstemmed | β-Arrestin1 Promotes Colorectal Cancer Metastasis Through GSK-3β/β-Catenin Signaling- Mediated Epithelial-to-Mesenchymal Transition |
title_short | β-Arrestin1 Promotes Colorectal Cancer Metastasis Through GSK-3β/β-Catenin Signaling- Mediated Epithelial-to-Mesenchymal Transition |
title_sort | β arrestin1 promotes colorectal cancer metastasis through gsk 3β β catenin signaling mediated epithelial to mesenchymal transition |
topic | colorectal cancer epithelial-to-mesenchymal transition metastasis β-arrestin1 Wnt/β-catenin signaling pathway |
url | https://www.frontiersin.org/articles/10.3389/fcell.2021.650067/full |
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