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SNORA71B promotes breast cancer cells across blood–brain barrier by inducing epithelial-mesenchymal transition

BACKGROUND: Brain metastasis (BM) is a dreadful complication that significantly impacts the quality of life in breast cancer patients. A key process during brain metastasis is the migration of cancer cells across blood–brain barrier (BBB). However, the role of snoRNAs regulating BBB in BM is still u...

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Autores principales: Duan, Sijia, Luo, Xuliang, Zeng, Huihui, Zhan, Xiang, Yuan, Chunlei
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Springer Japan 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7567732/
https://www.ncbi.nlm.nih.gov/pubmed/32458152
http://dx.doi.org/10.1007/s12282-020-01111-1
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author Duan, Sijia
Luo, Xuliang
Zeng, Huihui
Zhan, Xiang
Yuan, Chunlei
author_facet Duan, Sijia
Luo, Xuliang
Zeng, Huihui
Zhan, Xiang
Yuan, Chunlei
author_sort Duan, Sijia
collection PubMed
description BACKGROUND: Brain metastasis (BM) is a dreadful complication that significantly impacts the quality of life in breast cancer patients. A key process during brain metastasis is the migration of cancer cells across blood–brain barrier (BBB). However, the role of snoRNAs regulating BBB in BM is still unknown. METHODS: Here SNORic and GEO databases were used to identify differentially expressed snoRNAs between brain metastatic and non-metastatic breast cancer (BC) tissues. The effects of SNORA71B on the capacities of proliferation, migration, invasion, epithelial-mesenchymal transition (EMT), and BBB invasion of BC cells were evaluated by CCK8, transwell, western blot, and BBB model, respectively. RESULTS: SNORA71B was highly expressed in high BM BC tissues and cells compared to low BM BC controls. Survival analysis revealed high expression of SNORA71B was significantly associated with poor PPS and OS in breast cancer patients. ROC curve showed that SNORA71B might act as biomarker for breast cancer. Moreover, SNORA71B significantly promoted proliferation, migration, and invasion of BC cells with different BM abilities. Importantly, SNORA71B promoted the EMT process of low BM BC cells. SNORA71B knockdown inhibited the high BM BC cells across BBB, while EMT activator dramatically abrogated this inhibited effect. CONCLUSIONS: In conclusion, SNORA71B promotes BC cells across the BBB partly via inducing EMT.
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spelling pubmed-75677322020-10-19 SNORA71B promotes breast cancer cells across blood–brain barrier by inducing epithelial-mesenchymal transition Duan, Sijia Luo, Xuliang Zeng, Huihui Zhan, Xiang Yuan, Chunlei Breast Cancer Original Article BACKGROUND: Brain metastasis (BM) is a dreadful complication that significantly impacts the quality of life in breast cancer patients. A key process during brain metastasis is the migration of cancer cells across blood–brain barrier (BBB). However, the role of snoRNAs regulating BBB in BM is still unknown. METHODS: Here SNORic and GEO databases were used to identify differentially expressed snoRNAs between brain metastatic and non-metastatic breast cancer (BC) tissues. The effects of SNORA71B on the capacities of proliferation, migration, invasion, epithelial-mesenchymal transition (EMT), and BBB invasion of BC cells were evaluated by CCK8, transwell, western blot, and BBB model, respectively. RESULTS: SNORA71B was highly expressed in high BM BC tissues and cells compared to low BM BC controls. Survival analysis revealed high expression of SNORA71B was significantly associated with poor PPS and OS in breast cancer patients. ROC curve showed that SNORA71B might act as biomarker for breast cancer. Moreover, SNORA71B significantly promoted proliferation, migration, and invasion of BC cells with different BM abilities. Importantly, SNORA71B promoted the EMT process of low BM BC cells. SNORA71B knockdown inhibited the high BM BC cells across BBB, while EMT activator dramatically abrogated this inhibited effect. CONCLUSIONS: In conclusion, SNORA71B promotes BC cells across the BBB partly via inducing EMT. Springer Japan 2020-05-23 2020 /pmc/articles/PMC7567732/ /pubmed/32458152 http://dx.doi.org/10.1007/s12282-020-01111-1 Text en © The Author(s) 2020 Open AccessThis 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 licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence 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 licence, visit http://creativecommons.org/licenses/by/4.0/.
spellingShingle Original Article
Duan, Sijia
Luo, Xuliang
Zeng, Huihui
Zhan, Xiang
Yuan, Chunlei
SNORA71B promotes breast cancer cells across blood–brain barrier by inducing epithelial-mesenchymal transition
title SNORA71B promotes breast cancer cells across blood–brain barrier by inducing epithelial-mesenchymal transition
title_full SNORA71B promotes breast cancer cells across blood–brain barrier by inducing epithelial-mesenchymal transition
title_fullStr SNORA71B promotes breast cancer cells across blood–brain barrier by inducing epithelial-mesenchymal transition
title_full_unstemmed SNORA71B promotes breast cancer cells across blood–brain barrier by inducing epithelial-mesenchymal transition
title_short SNORA71B promotes breast cancer cells across blood–brain barrier by inducing epithelial-mesenchymal transition
title_sort snora71b promotes breast cancer cells across blood–brain barrier by inducing epithelial-mesenchymal transition
topic Original Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7567732/
https://www.ncbi.nlm.nih.gov/pubmed/32458152
http://dx.doi.org/10.1007/s12282-020-01111-1
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