Aurora B induces epithelial–mesenchymal transition by stabilizing Snail1 to promote basal-like breast cancer metastasis
Aurora B is a serine/threonine kinase that has been implicated in regulating cell proliferation in distinct cancers, including breast cancer. Here we show that Aurora B expression is elevated in basal-like breast cancer (BLBC) compared with other breast cancer subtypes. This high level of expression...
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Published in | Oncogene Vol. 39; no. 12; pp. 2550 - 2567 |
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Main Authors | , , , , , , |
Format | Journal Article |
Language | English |
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London
Nature Publishing Group UK
01.03.2020
Nature Publishing Group |
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Abstract | Aurora B is a serine/threonine kinase that has been implicated in regulating cell proliferation in distinct cancers, including breast cancer. Here we show that Aurora B expression is elevated in basal-like breast cancer (BLBC) compared with other breast cancer subtypes. This high level of expression seems to correlate with poor metastasis-free survival and relapse-free survival in affected patients. Mechanistically, we show that elevated Aurora B expression in breast cancer cells activates AKT/GSK3β to stabilize Snail1 protein, a master regulator of epithelial–mesenchymal transition (EMT), leading to EMT induction in a kinase-dependent manner. Conversely, Aurora B knock down by short-hairpin RNAs (shRNAs) suppresses AKT/GSK3β/Snail1 signaling, reverses EMT and reduces breast cancer metastatic potential in vitro and in vivo. Finally, we identified a specific OCT4 phosphorylation site (T343) responsible for mediating Aurora B-induced AKT/GSK3β/Snail1 signaling and EMT that could be attenuated by Aurora B kinase inhibitor treatment. These findings support that Aurora B induces EMT to promote breast cancer metastasis via OCT4/AKT/GSK3β/Snail1 signaling. Pharmacologic Aurora B inhibition might be a potential effective treatment for breast cancer patients with metastatic disease. |
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AbstractList | Aurora B is a serine/threonine kinase that has been implicated in regulating cell proliferation in distinct cancers, including breast cancer. Here we show that Aurora B expression is elevated in basal-like breast cancer (BLBC) compared with other breast cancer subtypes. This high level of expression seems to correlate with poor metastasis-free survival and relapse-free survival in affected patients. Mechanistically, we show that elevated Aurora B expression in breast cancer cells activates AKT/GSK3β to stabilize Snail1 protein, a master regulator of epithelial–mesenchymal transition (EMT), leading to EMT induction in a kinase-dependent manner. Conversely, Aurora B knock down by short-hairpin RNAs (shRNAs) suppresses AKT/GSK3β/Snail1 signaling, reverses EMT and reduces breast cancer metastatic potential in vitro and in vivo. Finally, we identified a specific OCT4 phosphorylation site (T343) responsible for mediating Aurora B-induced AKT/GSK3β/Snail1 signaling and EMT that could be attenuated by Aurora B kinase inhibitor treatment. These findings support that Aurora B induces EMT to promote breast cancer metastasis via OCT4/AKT/GSK3β/Snail1 signaling. Pharmacologic Aurora B inhibition might be a potential effective treatment for breast cancer patients with metastatic disease. Aurora B is a serine/threonine kinase that has been implicated in regulating cell proliferation in distinct cancers, including breast cancer. Here we show that Aurora B expression is elevated in basal-like breast cancer (BLBC) compared with other breast cancer subtypes. This high level of expression seems to correlate with poor metastasis-free survival and relapse-free survival in affected patients. Mechanistically, we show that elevated Aurora B expression in breast cancer cells activates AKT/GSK3[beta] to stabilize Snail1 protein, a master regulator of epithelial-mesenchymal transition (EMT), leading to EMT induction in a kinase-dependent manner. Conversely, Aurora B knock down by short-hairpin RNAs (shRNAs) suppresses AKT/GSK3[beta]/Snail1 signaling, reverses EMT and reduces breast cancer metastatic potential in vitro and in vivo. Finally, we identified a specific OCT4 phosphorylation site (T343) responsible for mediating Aurora B-induced AKT/GSK3[beta]/Snail1 signaling and EMT that could be attenuated by Aurora B kinase inhibitor treatment. These findings support that Aurora B induces EMT to promote breast cancer metastasis via OCT4/AKT/GSK3[beta]/Snail1 signaling. Pharmacologic Aurora B inhibition might be a potential effective treatment for breast cancer patients with metastatic disease. |
Audience | Academic |
Author | Huang, Jia-Jia Wu, Liufeng Lin, Xinxin Kipps, Thomas J. Zhang, Suping Jiang, Wen-Qi Zhang, Jianchao |
Author_xml | – sequence: 1 givenname: Jianchao surname: Zhang fullname: Zhang, Jianchao organization: Guangdong Key Laboratory for Genome Stability and Human Disease Prevention, Department of Pharmacology, Base for International Science and Technology Cooperation: Carson Cancer Stem Cell Vaccines R&D Center, International Cancer Center, Shenzhen University Health Science Center – sequence: 2 givenname: Xinxin surname: Lin fullname: Lin, Xinxin organization: Guangdong Key Laboratory for Genome Stability and Human Disease Prevention, Department of Pharmacology, Base for International Science and Technology Cooperation: Carson Cancer Stem Cell Vaccines R&D Center, International Cancer Center, Shenzhen University Health Science Center – sequence: 3 givenname: Liufeng surname: Wu fullname: Wu, Liufeng organization: Guangdong Key Laboratory for Genome Stability and Human Disease Prevention, Department of Pharmacology, Base for International Science and Technology Cooperation: Carson Cancer Stem Cell Vaccines R&D Center, International Cancer Center, Shenzhen University Health Science Center – sequence: 4 givenname: Jia-Jia surname: Huang fullname: Huang, Jia-Jia organization: State Key Laboratory of Oncology in South China, Department of Medical Oncology, Collaborative Innovation Center for Cancer Medicine, Sun Yat-sen University Cancer Center – sequence: 5 givenname: Wen-Qi surname: Jiang fullname: Jiang, Wen-Qi organization: State Key Laboratory of Oncology in South China, Department of Medical Oncology, Collaborative Innovation Center for Cancer Medicine, Sun Yat-sen University Cancer Center – sequence: 6 givenname: Thomas J. surname: Kipps fullname: Kipps, Thomas J. organization: Moores UCSD Cancer Center, University of California – sequence: 7 givenname: Suping surname: Zhang fullname: Zhang, Suping email: s9zhang@szu.edu.cn organization: Guangdong Key Laboratory for Genome Stability and Human Disease Prevention, Department of Pharmacology, Base for International Science and Technology Cooperation: Carson Cancer Stem Cell Vaccines R&D Center, International Cancer Center, Shenzhen University Health Science Center, Moores UCSD Cancer Center, University of California |
BackLink | https://www.ncbi.nlm.nih.gov/pubmed/31996785$$D View this record in MEDLINE/PubMed |
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Snippet | Aurora B is a serine/threonine kinase that has been implicated in regulating cell proliferation in distinct cancers, including breast cancer. Here we show that... |
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SubjectTerms | 13 13/1 13/105 13/109 13/44 13/51 13/89 13/95 14/34 38/22 59 59/5 631/67/395 64 692/53/2423 82 AKT protein Animals Apoptosis Aurora B protein Aurora Kinase B - antagonists & inhibitors Aurora Kinase B - metabolism Breast cancer Breast Neoplasms - metabolism Breast Neoplasms - pathology Carcinoma, Ductal - metabolism Carcinoma, Ductal - pathology Care and treatment Cell Biology Cell Line, Tumor Cell proliferation Complications and side effects Down-Regulation Enzyme inhibitors Epithelial-Mesenchymal Transition Female Gene expression Genetic aspects Glycogen Synthase Kinase 3 beta - metabolism Health aspects Human Genetics Humans Internal Medicine Kinases Lung Neoplasms - secondary Medicine Medicine & Public Health Mesenchyme Metastases Metastasis Mice Mice, Inbred NOD Neoplasm Invasiveness Neoplasm Metastasis Oct-4 protein Octamer Transcription Factor-3 - metabolism Oncology Organophosphates - pharmacology Phosphorylation Phosphotransferases Protein Kinase Inhibitors - pharmacology Protein Stability Protein-serine/threonine kinase Quinazolines - pharmacology Risk factors Signal Transduction Snail Family Transcription Factors - metabolism Triple Negative Breast Neoplasms - metabolism |
Title | Aurora B induces epithelial–mesenchymal transition by stabilizing Snail1 to promote basal-like breast cancer metastasis |
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