Loss of Gap Junction Factor Connexin 43 Results in an Increase of Exosomal Tetraspanins in Human Lung Cancer Cell Line A549

Gap junctions (GJs) and small extracellular vesicles such as exosomes are two fundamental intercellular communication (IC) mechanisms. We tested the hypothesis that the two IC mechanisms are connected by gene editing to inactivate a ubiquitously expression GJ factor (i.e., Cx43) in the human lung ca...

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Detalles Bibliográficos
Autores principales: Fleck, Alexandra P, Flotte, Ariel B, Si, Edward P, Mu, David
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Caltech Library 2022
Materias:
New Finding
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9701318/
https://www.ncbi.nlm.nih.gov/pubmed/36447528
http://dx.doi.org/10.17912/micropub.biology.000683
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author Fleck, Alexandra P
Flotte, Ariel B
Si, Edward P
Mu, David
author_facet Fleck, Alexandra P
Flotte, Ariel B
Si, Edward P
Mu, David
author_sort Fleck, Alexandra P
collection PubMed
description Gap junctions (GJs) and small extracellular vesicles such as exosomes are two fundamental intercellular communication (IC) mechanisms. We tested the hypothesis that the two IC mechanisms are connected by gene editing to inactivate a ubiquitously expression GJ factor (i.e., Cx43) in the human lung cancer cell line A549. Surprisingly, we observed that loss of Cx43 led to a buildup of exosomal tetraspanin proteins such as CD63 and CD9. Given the known activities of tetraspanins in cell-cell adhesion and vesicle uptake, our observation establishes an impetus to investigate further how these two IC mechanisms are intertwined
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spelling pubmed-97013182022-11-28 Loss of Gap Junction Factor Connexin 43 Results in an Increase of Exosomal Tetraspanins in Human Lung Cancer Cell Line A549 Fleck, Alexandra P Flotte, Ariel B Si, Edward P Mu, David MicroPubl Biol New Finding Gap junctions (GJs) and small extracellular vesicles such as exosomes are two fundamental intercellular communication (IC) mechanisms. We tested the hypothesis that the two IC mechanisms are connected by gene editing to inactivate a ubiquitously expression GJ factor (i.e., Cx43) in the human lung cancer cell line A549. Surprisingly, we observed that loss of Cx43 led to a buildup of exosomal tetraspanin proteins such as CD63 and CD9. Given the known activities of tetraspanins in cell-cell adhesion and vesicle uptake, our observation establishes an impetus to investigate further how these two IC mechanisms are intertwined Caltech Library 2022-11-13 /pmc/articles/PMC9701318/ /pubmed/36447528 http://dx.doi.org/10.17912/micropub.biology.000683 Text en Copyright: © 2022 by the authors https://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 credited.
spellingShingle New Finding
Fleck, Alexandra P
Flotte, Ariel B
Si, Edward P
Mu, David
Loss of Gap Junction Factor Connexin 43 Results in an Increase of Exosomal Tetraspanins in Human Lung Cancer Cell Line A549
title Loss of Gap Junction Factor Connexin 43 Results in an Increase of Exosomal Tetraspanins in Human Lung Cancer Cell Line A549
title_full Loss of Gap Junction Factor Connexin 43 Results in an Increase of Exosomal Tetraspanins in Human Lung Cancer Cell Line A549
title_fullStr Loss of Gap Junction Factor Connexin 43 Results in an Increase of Exosomal Tetraspanins in Human Lung Cancer Cell Line A549
title_full_unstemmed Loss of Gap Junction Factor Connexin 43 Results in an Increase of Exosomal Tetraspanins in Human Lung Cancer Cell Line A549
title_short Loss of Gap Junction Factor Connexin 43 Results in an Increase of Exosomal Tetraspanins in Human Lung Cancer Cell Line A549
title_sort loss of gap junction factor connexin 43 results in an increase of exosomal tetraspanins in human lung cancer cell line a549
topic New Finding
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9701318/
https://www.ncbi.nlm.nih.gov/pubmed/36447528
http://dx.doi.org/10.17912/micropub.biology.000683
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