dc.creator | Jardín, Isaac | es |
dc.creator | Diez Bello, Raquel | es |
dc.creator | Lopez, Jose J. | es |
dc.creator | Redondo, Pedro C. | es |
dc.creator | Salido, Gines M. | es |
dc.creator | Smani Hajami, Tarik | es |
dc.creator | Rosado, Juan Antonio | es |
dc.date.accessioned | 2018-10-05T07:29:53Z | |
dc.date.available | 2018-10-05T07:29:53Z | |
dc.date.issued | 2018-09-14 | |
dc.identifier.citation | Jardín, I., Diez Bello, R., Lopez, J.J., Redondo, P.C., Salido, G.M., Smani Hajami, T. y Rosado, J.A. (2018). TRPC6 channels are required for proliferation, migration and invasion of breast cancer cell lines by modulation of Orai1 and Orai3 surface exposure. Cancers, 10 (9) | |
dc.identifier.issn | 2072-6694 | es |
dc.identifier.uri | https://hdl.handle.net/11441/79103 | |
dc.description.abstract | Transient receptor potential channels convey signaling information from a number of stimuli to a wide variety of cellular functions, mainly by inducing changes in cytosolic Ca2+ concentration. Different members of the TRPC, TRPM and TRPV subfamilies have been reported to play a role in tumorigenesis. Here we show that the estrogen receptor positive and triple negative breast cancer cell lines, MCF7 and MDA-MB-231, respectively, exhibit enhanced expression of the TRPC6 channel as compared to the non-tumoral MCF10A cell line. In vitro TRPC6 knockdown using shRNA impaired MCF7 and MDA-MB-231 cell proliferation, migration and invasion detected by BrdU incorporation, wound healing and Boyden chamber assays, respectively. Using RNAi-mediated TRPC6 silencing as well as overexpression of the pore-dead dominant-negative TRPC6 mutant we have found that TRPC6 plays a relevant role in the activation of store-operated Ca2+ entry in the breast cancer cell lines but not in non-tumoral breast cells. Finally, we have found that TRPC6 interacts with Orai1 and Orai3 in MCF7 and MDA-MB-231 cells and is required for the translocation of Orai1 and Orai3 to the plasma membrane in MDA-MB-231 and MCF7 cells, respectively, upon Ca2+ store depletion. These findings introduce a novel mechanism for the modulation of Ca2+ influx and the development of different cancer hallmarks in breast cancer cells. | es |
dc.format | application/pdf | es |
dc.language.iso | eng | es |
dc.publisher | MDPI AC | es |
dc.relation.ispartof | Cancers, 10 (9) | |
dc.rights | Attribution-NonCommercial-NoDerivatives 4.0 Internacional | * |
dc.rights.uri | http://creativecommons.org/licenses/by-nc-nd/4.0/ | * |
dc.subject | TRPC6 | es |
dc.subject | Orai1 | es |
dc.subject | Orai3 | es |
dc.subject | Store-operated calcium entry | es |
dc.subject | MCF7 | es |
dc.subject | MDA-MB-231 | es |
dc.title | TRPC6 channels are required for proliferation, migration and invasion of breast cancer cell lines by modulation of Orai1 and Orai3 surface exposure | es |
dc.type | info:eu-repo/semantics/article | es |
dcterms.identifier | https://ror.org/03yxnpp24 | |
dc.type.version | info:eu-repo/semantics/publishedVersion | es |
dc.rights.accessRights | info:eu-repo/semantics/openAccess | es |
dc.contributor.affiliation | Universidad de Sevilla. Departamento de Fisiología Médica y Biofísica | es |
dc.relation.publisherversion | https://doi.org/10.3390/cancers10090331 | es |
dc.identifier.doi | 10.3390/cancers10090331 | es |
idus.format.extent | 18 | es |
dc.journaltitle | Cancers | es |
dc.publication.volumen | 10 | es |
dc.publication.issue | 9 | es |