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Human Equilibrative Nucleoside Transporter-1 Knockdown Tunes Cellular Mechanics through Epithelial-Mesenchymal Transition in Pancreatic Cancer Cells
We report cell mechanical changes in response to alteration of expression of the human equilibrative nucleoside transporter-1 (hENT1), a most abundant and widely distributed plasma membrane nucleoside transporter in human cells and/or tissues. Modulation of hENT1 expression level altered the stiffne...
Autores principales: | , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Public Library of Science
2014
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4196761/ https://www.ncbi.nlm.nih.gov/pubmed/25314577 http://dx.doi.org/10.1371/journal.pone.0107973 |
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author | Lee, Yeonju Koay, Eugene J. Zhang, Weijia Qin, Lidong Kirui, Dickson K. Hussain, Fazle Shen, Haifa Ferrari, Mauro |
author_facet | Lee, Yeonju Koay, Eugene J. Zhang, Weijia Qin, Lidong Kirui, Dickson K. Hussain, Fazle Shen, Haifa Ferrari, Mauro |
author_sort | Lee, Yeonju |
collection | PubMed |
description | We report cell mechanical changes in response to alteration of expression of the human equilibrative nucleoside transporter-1 (hENT1), a most abundant and widely distributed plasma membrane nucleoside transporter in human cells and/or tissues. Modulation of hENT1 expression level altered the stiffness of pancreatic cancer Capan-1 and Panc 03.27 cells, which was analyzed by atomic force microscopy (AFM) and correlated to microfluidic platform. The hENT1 knockdown induced reduction of cellular stiffness in both of cells up to 70%. In addition, cellular phenotypic changes such as cell morphology, migration, and expression level of epithelial-mesenchymal transition (EMT) markers were observed after hENT1 knockdown. Cells with suppressed hENT1 became elongated, migrated faster, and had reduced E-cadherin and elevated N-cadherin compared to parental cells which are consistent with epithelial-mesenchymal transition (EMT). Those cellular phenotypic changes closely correlated with changes in cellular stiffness. This study suggests that hENT1 expression level affects cellular phenotype and cell elastic behavior can be a physical biomarker for quantify hENT1 expression and detect phenotypic shift. Furthermore, cell mechanics can be a critical tool in detecting disease progression and response to therapy. |
format | Online Article Text |
id | pubmed-4196761 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2014 |
publisher | Public Library of Science |
record_format | MEDLINE/PubMed |
spelling | pubmed-41967612014-10-16 Human Equilibrative Nucleoside Transporter-1 Knockdown Tunes Cellular Mechanics through Epithelial-Mesenchymal Transition in Pancreatic Cancer Cells Lee, Yeonju Koay, Eugene J. Zhang, Weijia Qin, Lidong Kirui, Dickson K. Hussain, Fazle Shen, Haifa Ferrari, Mauro PLoS One Research Article We report cell mechanical changes in response to alteration of expression of the human equilibrative nucleoside transporter-1 (hENT1), a most abundant and widely distributed plasma membrane nucleoside transporter in human cells and/or tissues. Modulation of hENT1 expression level altered the stiffness of pancreatic cancer Capan-1 and Panc 03.27 cells, which was analyzed by atomic force microscopy (AFM) and correlated to microfluidic platform. The hENT1 knockdown induced reduction of cellular stiffness in both of cells up to 70%. In addition, cellular phenotypic changes such as cell morphology, migration, and expression level of epithelial-mesenchymal transition (EMT) markers were observed after hENT1 knockdown. Cells with suppressed hENT1 became elongated, migrated faster, and had reduced E-cadherin and elevated N-cadherin compared to parental cells which are consistent with epithelial-mesenchymal transition (EMT). Those cellular phenotypic changes closely correlated with changes in cellular stiffness. This study suggests that hENT1 expression level affects cellular phenotype and cell elastic behavior can be a physical biomarker for quantify hENT1 expression and detect phenotypic shift. Furthermore, cell mechanics can be a critical tool in detecting disease progression and response to therapy. Public Library of Science 2014-10-14 /pmc/articles/PMC4196761/ /pubmed/25314577 http://dx.doi.org/10.1371/journal.pone.0107973 Text en © 2014 Lee et al http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are properly credited. |
spellingShingle | Research Article Lee, Yeonju Koay, Eugene J. Zhang, Weijia Qin, Lidong Kirui, Dickson K. Hussain, Fazle Shen, Haifa Ferrari, Mauro Human Equilibrative Nucleoside Transporter-1 Knockdown Tunes Cellular Mechanics through Epithelial-Mesenchymal Transition in Pancreatic Cancer Cells |
title | Human Equilibrative Nucleoside Transporter-1 Knockdown Tunes Cellular Mechanics through Epithelial-Mesenchymal Transition in Pancreatic Cancer Cells |
title_full | Human Equilibrative Nucleoside Transporter-1 Knockdown Tunes Cellular Mechanics through Epithelial-Mesenchymal Transition in Pancreatic Cancer Cells |
title_fullStr | Human Equilibrative Nucleoside Transporter-1 Knockdown Tunes Cellular Mechanics through Epithelial-Mesenchymal Transition in Pancreatic Cancer Cells |
title_full_unstemmed | Human Equilibrative Nucleoside Transporter-1 Knockdown Tunes Cellular Mechanics through Epithelial-Mesenchymal Transition in Pancreatic Cancer Cells |
title_short | Human Equilibrative Nucleoside Transporter-1 Knockdown Tunes Cellular Mechanics through Epithelial-Mesenchymal Transition in Pancreatic Cancer Cells |
title_sort | human equilibrative nucleoside transporter-1 knockdown tunes cellular mechanics through epithelial-mesenchymal transition in pancreatic cancer cells |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4196761/ https://www.ncbi.nlm.nih.gov/pubmed/25314577 http://dx.doi.org/10.1371/journal.pone.0107973 |
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