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Upregulation of CD109 Promotes the Epithelial-to-Mesenchymal Transition and Stemness Properties of Lung Adenocarcinomas via Activation of the Hippo-YAP Signaling

Metastasis is the leading cause of death in lung adenocarcinomas. Identifying potential prognostic biomarkers and exploiting regulatory mechanisms could improve the diagnosis and treatment of lung cancer patients. We previously found that cluster of differentiation 109 (CD109) was upregulated in lun...

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Autores principales: Lee, Kang-Yun, Kuo, Tai-Chih, Chou, Chih-Ming, Hsu, Wen-Jing, Lee, Wei-Cheng, Dai, Jia-Zih, Wu, Sheng-Ming, Lin, Cheng-Wei
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7823273/
https://www.ncbi.nlm.nih.gov/pubmed/33375719
http://dx.doi.org/10.3390/cells10010028
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author Lee, Kang-Yun
Kuo, Tai-Chih
Chou, Chih-Ming
Hsu, Wen-Jing
Lee, Wei-Cheng
Dai, Jia-Zih
Wu, Sheng-Ming
Lin, Cheng-Wei
author_facet Lee, Kang-Yun
Kuo, Tai-Chih
Chou, Chih-Ming
Hsu, Wen-Jing
Lee, Wei-Cheng
Dai, Jia-Zih
Wu, Sheng-Ming
Lin, Cheng-Wei
author_sort Lee, Kang-Yun
collection PubMed
description Metastasis is the leading cause of death in lung adenocarcinomas. Identifying potential prognostic biomarkers and exploiting regulatory mechanisms could improve the diagnosis and treatment of lung cancer patients. We previously found that cluster of differentiation 109 (CD109) was upregulated in lung tumor tissues, and CD109 overexpression was correlated with the invasive and metastatic capacities of lung adenocarcinoma cells. However, the contribution of CD109 to lung tumorigenesis remains to be elucidated. In the present study, we identified that CD109 was upregulated in metastatic lung adenocarcinoma cells, and elevation of CD109 was correlated with epithelial-to-mesenchymal transition (EMT) traits in patients with lung adenocarcinoma. Functionally, CD109 expression was crucial for EMT gene expressions, tumor invasiveness, and cancer stemness properties. Moreover, elevation of CD109 was accompanied by upregulation of the yes-associated protein (YAP) signature in metastatic lung cancer cells and lung cancer patients, and activation of YAP was demonstrated to participate in CD109-elicited EMT gene expressions and tumor invasiveness. Our study reveals the molecular mechanism underlying CD109 in lung tumor aggressiveness, and CD109 could be a potential diagnostic and therapeutic target for lung cancer patients.
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spelling pubmed-78232732021-01-24 Upregulation of CD109 Promotes the Epithelial-to-Mesenchymal Transition and Stemness Properties of Lung Adenocarcinomas via Activation of the Hippo-YAP Signaling Lee, Kang-Yun Kuo, Tai-Chih Chou, Chih-Ming Hsu, Wen-Jing Lee, Wei-Cheng Dai, Jia-Zih Wu, Sheng-Ming Lin, Cheng-Wei Cells Article Metastasis is the leading cause of death in lung adenocarcinomas. Identifying potential prognostic biomarkers and exploiting regulatory mechanisms could improve the diagnosis and treatment of lung cancer patients. We previously found that cluster of differentiation 109 (CD109) was upregulated in lung tumor tissues, and CD109 overexpression was correlated with the invasive and metastatic capacities of lung adenocarcinoma cells. However, the contribution of CD109 to lung tumorigenesis remains to be elucidated. In the present study, we identified that CD109 was upregulated in metastatic lung adenocarcinoma cells, and elevation of CD109 was correlated with epithelial-to-mesenchymal transition (EMT) traits in patients with lung adenocarcinoma. Functionally, CD109 expression was crucial for EMT gene expressions, tumor invasiveness, and cancer stemness properties. Moreover, elevation of CD109 was accompanied by upregulation of the yes-associated protein (YAP) signature in metastatic lung cancer cells and lung cancer patients, and activation of YAP was demonstrated to participate in CD109-elicited EMT gene expressions and tumor invasiveness. Our study reveals the molecular mechanism underlying CD109 in lung tumor aggressiveness, and CD109 could be a potential diagnostic and therapeutic target for lung cancer patients. MDPI 2020-12-25 /pmc/articles/PMC7823273/ /pubmed/33375719 http://dx.doi.org/10.3390/cells10010028 Text en © 2020 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).
spellingShingle Article
Lee, Kang-Yun
Kuo, Tai-Chih
Chou, Chih-Ming
Hsu, Wen-Jing
Lee, Wei-Cheng
Dai, Jia-Zih
Wu, Sheng-Ming
Lin, Cheng-Wei
Upregulation of CD109 Promotes the Epithelial-to-Mesenchymal Transition and Stemness Properties of Lung Adenocarcinomas via Activation of the Hippo-YAP Signaling
title Upregulation of CD109 Promotes the Epithelial-to-Mesenchymal Transition and Stemness Properties of Lung Adenocarcinomas via Activation of the Hippo-YAP Signaling
title_full Upregulation of CD109 Promotes the Epithelial-to-Mesenchymal Transition and Stemness Properties of Lung Adenocarcinomas via Activation of the Hippo-YAP Signaling
title_fullStr Upregulation of CD109 Promotes the Epithelial-to-Mesenchymal Transition and Stemness Properties of Lung Adenocarcinomas via Activation of the Hippo-YAP Signaling
title_full_unstemmed Upregulation of CD109 Promotes the Epithelial-to-Mesenchymal Transition and Stemness Properties of Lung Adenocarcinomas via Activation of the Hippo-YAP Signaling
title_short Upregulation of CD109 Promotes the Epithelial-to-Mesenchymal Transition and Stemness Properties of Lung Adenocarcinomas via Activation of the Hippo-YAP Signaling
title_sort upregulation of cd109 promotes the epithelial-to-mesenchymal transition and stemness properties of lung adenocarcinomas via activation of the hippo-yap signaling
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7823273/
https://www.ncbi.nlm.nih.gov/pubmed/33375719
http://dx.doi.org/10.3390/cells10010028
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