Correction: Gap junction-mediated transfer of miR-145-5p from microvascular endothelial cells to colon cancer cells inhibits angiogenesis

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Oncotarget. 2024; 15:285-287. https://doi.org/10.18632/oncotarget.28528

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Dominique Thuringer1, Gaetan Jego1,2, Kevin Berthenet1, Arlette Hammann1, Eric Solary3 and Carmen Garrido1,2,4

1INSERM, U866, Faculty of Medecine, 21000 Dijon, France
2University of Bourgogne-Franche-Comté, 21000 Dijon, France
3INSERM, U1170, Institut Gustave Roussy, 94508 Villejuif, France
4CGFL, BP77980, 21000 Dijon, France

Published: May 07, 2024

Copyright: © 2024 Thuringer et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

This article has been corrected: Because a previously published image was used in Figure 1E, the authors have updated the figure legend as shown below. The authors declare that these corrections do not change the results or conclusions of this paper.

Original article: Oncotarget. 2016; 7:28160–28168. DOI: https://doi.org/10.18632/oncotarget.8583

Figure 1: Micro-RNA transfer from microvascular endothelium (HMEC) to colorectal cancer cells (SW480). (A) Expression profile of miR-145 in HMEC (black) and SW480 (hatched), separately cultured (left) or co-cultured (right) for 12 hours. Levels of miR-145 were expressed relative to levels of U6 snRNA, commonly used as an internal control in miRs analysis (means ± SD; * P < 0.05; n = 3). (B) Cell sorting by flow cytometry. SW480 were labelled with the fluorescent dye DiL-C18 (red cells), then plated with unlabeled HMEC in a ratio of 1:1. (C) Scheme illustrating the procedure to determine the transfer of microRNA (miR-145) through heterocellular gap junction channels established between HMEC and SW480. (D) Transfer of miR-145 to SW480 is inhibited by a gap junction blocker. HMEC loaded with miR-145-5p mimic (30 nM) were co-cultured with SW480, in the presence or the absence of carbenoxolone (carb. 100 µM). The miR-145 levels measured in donor HMEC (black) and receiver SW480 (hatched), after 12 h of co-culture. Note that carbenoxolone does not affect the miR-145 expression in transfected HMEC or in cancer cells cultured separately. (E) Down-regulation of Cx43 expression in HMEC does not affect loading of miR-145 mimic but suppresses transfer of miR-145 to SW480. Right insert, representative immune-blot of Cx43 protein level in HMEC transfected with control siRNA or siRNA Cx43 ([28]; Hsc70 as loading control). Note that the siRNA Cx43 transfection of HMEC does not affect their loading with miR-145-5p mimic. D, E. Values of miR-1455p expression relative to U6 snRNA in each cell type and condition, are means ± SD of triplicate measurements from three experiments; * P < 0.5 vs. donors (Mann-Whitney U test and Kruskal-Wallis test; n = 3).


28. Thuringer D, Berthenet K, Cronier L, Jego G, Solary E, Garrido C. Oncogenic extracellular HSP70 disrupts the gap-junctional coupling between capillary cells. Oncotarget. 2015; 6:10267–83. https://doi.org/10.18632/oncotarget.3522. [PubMed]

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