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Downregulation of RAI14 inhibits the proliferation and invasion of breast cancer cells

Retinoic acid-induced 14 (RAI14) is involved in the development of different tumor types, however, its expression and biological function in breast cancer are yet unknown. In the current study, we demonstrated that RAI14 was highly expressed in breast cancer. The high expression of RAI14 is positive...

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Autores principales: Gu, Ming, Zheng, Wenhui, Zhang, Mingdi, Dong, Xiaoshen, Zhao, Yan, Wang, Shuo, Jiang, Haiyang, Liu, Lu, Zheng, Xinyu
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Ivyspring International Publisher 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6856746/
https://www.ncbi.nlm.nih.gov/pubmed/31772666
http://dx.doi.org/10.7150/jca.34910
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author Gu, Ming
Zheng, Wenhui
Zhang, Mingdi
Dong, Xiaoshen
Zhao, Yan
Wang, Shuo
Jiang, Haiyang
Liu, Lu
Zheng, Xinyu
author_facet Gu, Ming
Zheng, Wenhui
Zhang, Mingdi
Dong, Xiaoshen
Zhao, Yan
Wang, Shuo
Jiang, Haiyang
Liu, Lu
Zheng, Xinyu
author_sort Gu, Ming
collection PubMed
description Retinoic acid-induced 14 (RAI14) is involved in the development of different tumor types, however, its expression and biological function in breast cancer are yet unknown. In the current study, we demonstrated that RAI14 was highly expressed in breast cancer. The high expression of RAI14 is positively correlated with the malignant progression of breast cancer and suggests a worse prognosis. Further, we found that knockdown RAI14 inhibits the proliferation, migration and invasion of breast cancer cells by regulating cell cycle and EMT through Akt/Cyclin D1, MMP2, MMP9 and ZEB1/E-cadhrin/Vimentin pathway. These findings revealed a novel function for RAI14 in breast cancer progression and suggest that RAI14 may become a promising diagnostic and therapeutic target for breast cancer.
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spelling pubmed-68567462019-11-26 Downregulation of RAI14 inhibits the proliferation and invasion of breast cancer cells Gu, Ming Zheng, Wenhui Zhang, Mingdi Dong, Xiaoshen Zhao, Yan Wang, Shuo Jiang, Haiyang Liu, Lu Zheng, Xinyu J Cancer Research Paper Retinoic acid-induced 14 (RAI14) is involved in the development of different tumor types, however, its expression and biological function in breast cancer are yet unknown. In the current study, we demonstrated that RAI14 was highly expressed in breast cancer. The high expression of RAI14 is positively correlated with the malignant progression of breast cancer and suggests a worse prognosis. Further, we found that knockdown RAI14 inhibits the proliferation, migration and invasion of breast cancer cells by regulating cell cycle and EMT through Akt/Cyclin D1, MMP2, MMP9 and ZEB1/E-cadhrin/Vimentin pathway. These findings revealed a novel function for RAI14 in breast cancer progression and suggest that RAI14 may become a promising diagnostic and therapeutic target for breast cancer. Ivyspring International Publisher 2019-10-18 /pmc/articles/PMC6856746/ /pubmed/31772666 http://dx.doi.org/10.7150/jca.34910 Text en © The author(s) This is an open access article distributed under the terms of the Creative Commons Attribution License (https://creativecommons.org/licenses/by/4.0/). See http://ivyspring.com/terms for full terms and conditions.
spellingShingle Research Paper
Gu, Ming
Zheng, Wenhui
Zhang, Mingdi
Dong, Xiaoshen
Zhao, Yan
Wang, Shuo
Jiang, Haiyang
Liu, Lu
Zheng, Xinyu
Downregulation of RAI14 inhibits the proliferation and invasion of breast cancer cells
title Downregulation of RAI14 inhibits the proliferation and invasion of breast cancer cells
title_full Downregulation of RAI14 inhibits the proliferation and invasion of breast cancer cells
title_fullStr Downregulation of RAI14 inhibits the proliferation and invasion of breast cancer cells
title_full_unstemmed Downregulation of RAI14 inhibits the proliferation and invasion of breast cancer cells
title_short Downregulation of RAI14 inhibits the proliferation and invasion of breast cancer cells
title_sort downregulation of rai14 inhibits the proliferation and invasion of breast cancer cells
topic Research Paper
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6856746/
https://www.ncbi.nlm.nih.gov/pubmed/31772666
http://dx.doi.org/10.7150/jca.34910
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