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Palladin promotes cancer stem cell‐like properties in lung cancer by activating Wnt/Β‐Catenin signaling

BACKGROUND: Cancer stem cells (CSCs) are responsible for drug resistance, cancer relapse, and metastasis. Here, we report the first analysis of Palladin expression and its impacts on stem cell‐like properties in lung cancer. METHODS: Tissue microarrays were used to investigate Palladin expression an...

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Autores principales: Shu, Xiong, Chen, Meng, Liu, Shi‐Ya, Yu, Long, Sun, Li‐Xin, Sun, Li‐Chao, Ran, Yu‐Liang
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley and Sons Inc. 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9972019/
https://www.ncbi.nlm.nih.gov/pubmed/36047666
http://dx.doi.org/10.1002/cam4.5192
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author Shu, Xiong
Chen, Meng
Liu, Shi‐Ya
Yu, Long
Sun, Li‐Xin
Sun, Li‐Chao
Ran, Yu‐Liang
author_facet Shu, Xiong
Chen, Meng
Liu, Shi‐Ya
Yu, Long
Sun, Li‐Xin
Sun, Li‐Chao
Ran, Yu‐Liang
author_sort Shu, Xiong
collection PubMed
description BACKGROUND: Cancer stem cells (CSCs) are responsible for drug resistance, cancer relapse, and metastasis. Here, we report the first analysis of Palladin expression and its impacts on stem cell‐like properties in lung cancer. METHODS: Tissue microarrays were used to investigate Palladin expression and its association with prognosis. Immunofluorescence (IF), flow fluorescence assay, and Western blot were performed to detect Palladin expression in 6 NSCLC cell lines. Cell phenotypes and drug resistance were evaluated. Xenograft models were constructed to confirm the role of Palladin in vivo. RESULTS: By using the tissue microarrays, Palladin was identified to be highly expressed in the cytoplasm, specifically in the cytomembrane of NSCLC, and its high expression is associated with poor prognosis. Palladin is widely expressed and enriched in the sphere cells. The in vitro and in vivo studies showed that Palladin promoted stem cell‐like properties, including cell viability, invasion, migration, self‐renewal abilities, taxol resistance, and tumorigenicity. Western blot revealed that Palladin promoted the accumulation of β‐catenin and activated Wnt/β‐catenin signaling. Tissue microarrays analysis further confirmed the positive correlation between Palladin and β‐catenin. Wnt/β‐catenin pathway inhibitor blocked the Palladin‐induced enhancement of sphere‐forming. CONCLUSIONS: Palladin might act as an oncogene by promoting CSCs‐like properties and tumorigenicity of NSCLC cells via the Wnt/β‐catenin signaling pathway. Besides, Palladin was identified to have the potential as a cell surface marker for LCSCs identification. These findings provide a possible target for developing putative agents targeted to LCSCs.
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spelling pubmed-99720192023-03-01 Palladin promotes cancer stem cell‐like properties in lung cancer by activating Wnt/Β‐Catenin signaling Shu, Xiong Chen, Meng Liu, Shi‐Ya Yu, Long Sun, Li‐Xin Sun, Li‐Chao Ran, Yu‐Liang Cancer Med RESEARCH ARTICLES BACKGROUND: Cancer stem cells (CSCs) are responsible for drug resistance, cancer relapse, and metastasis. Here, we report the first analysis of Palladin expression and its impacts on stem cell‐like properties in lung cancer. METHODS: Tissue microarrays were used to investigate Palladin expression and its association with prognosis. Immunofluorescence (IF), flow fluorescence assay, and Western blot were performed to detect Palladin expression in 6 NSCLC cell lines. Cell phenotypes and drug resistance were evaluated. Xenograft models were constructed to confirm the role of Palladin in vivo. RESULTS: By using the tissue microarrays, Palladin was identified to be highly expressed in the cytoplasm, specifically in the cytomembrane of NSCLC, and its high expression is associated with poor prognosis. Palladin is widely expressed and enriched in the sphere cells. The in vitro and in vivo studies showed that Palladin promoted stem cell‐like properties, including cell viability, invasion, migration, self‐renewal abilities, taxol resistance, and tumorigenicity. Western blot revealed that Palladin promoted the accumulation of β‐catenin and activated Wnt/β‐catenin signaling. Tissue microarrays analysis further confirmed the positive correlation between Palladin and β‐catenin. Wnt/β‐catenin pathway inhibitor blocked the Palladin‐induced enhancement of sphere‐forming. CONCLUSIONS: Palladin might act as an oncogene by promoting CSCs‐like properties and tumorigenicity of NSCLC cells via the Wnt/β‐catenin signaling pathway. Besides, Palladin was identified to have the potential as a cell surface marker for LCSCs identification. These findings provide a possible target for developing putative agents targeted to LCSCs. John Wiley and Sons Inc. 2022-09-01 /pmc/articles/PMC9972019/ /pubmed/36047666 http://dx.doi.org/10.1002/cam4.5192 Text en © 2022 The Authors. Cancer Medicine published by John Wiley & Sons Ltd. https://creativecommons.org/licenses/by/4.0/This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.
spellingShingle RESEARCH ARTICLES
Shu, Xiong
Chen, Meng
Liu, Shi‐Ya
Yu, Long
Sun, Li‐Xin
Sun, Li‐Chao
Ran, Yu‐Liang
Palladin promotes cancer stem cell‐like properties in lung cancer by activating Wnt/Β‐Catenin signaling
title Palladin promotes cancer stem cell‐like properties in lung cancer by activating Wnt/Β‐Catenin signaling
title_full Palladin promotes cancer stem cell‐like properties in lung cancer by activating Wnt/Β‐Catenin signaling
title_fullStr Palladin promotes cancer stem cell‐like properties in lung cancer by activating Wnt/Β‐Catenin signaling
title_full_unstemmed Palladin promotes cancer stem cell‐like properties in lung cancer by activating Wnt/Β‐Catenin signaling
title_short Palladin promotes cancer stem cell‐like properties in lung cancer by activating Wnt/Β‐Catenin signaling
title_sort palladin promotes cancer stem cell‐like properties in lung cancer by activating wnt/β‐catenin signaling
topic RESEARCH ARTICLES
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9972019/
https://www.ncbi.nlm.nih.gov/pubmed/36047666
http://dx.doi.org/10.1002/cam4.5192
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