dc.creator | Sánchez-Collado, José | es |
dc.creator | Nieto-Felipe, Joel | es |
dc.creator | Jardín, Isaac | es |
dc.creator | Bhardwaj, Rajesh | es |
dc.creator | Berna-Erro, Alejandro | es |
dc.creator | Salido, Ginés M. | es |
dc.creator | Smani Hajami, Tarik | es |
dc.creator | Rosado, Juan A. | es |
dc.date.accessioned | 2023-05-31T13:09:28Z | |
dc.date.available | 2023-05-31T13:09:28Z | |
dc.date.issued | 2022-12-29 | |
dc.identifier.citation | Sánchez-Collado, J., Nieto-Felipe, J., Jardín, I., Bhardwaj, R., Berna-Erro, A., Salido, G.M.,...,Rosado, J.A. (2022). Store-operated calcium entry in breast cancer cells is insensitive to Orai1 and STIM1 N-linked glycosylation. CANCERS, 15 (1), 203. https://doi.org/10.3390/cancers15010203. | |
dc.identifier.issn | 2072-6694 | es |
dc.identifier.uri | https://hdl.handle.net/11441/146822 | |
dc.description.abstract | N-linked glycosylation is a post-translational modification that affects protein function,
structure, and interaction with other proteins. The store-operated Ca2+ entry (SOCE) core proteins,
Orai1 and STIM1, exhibit N-glycosylation consensus motifs. Abnormal SOCE has been associated to
a number of disorders, including cancer, and alterations in Orai1 glycosylation have been related to
cancer invasiveness and metastasis. Here we show that treatment of non-tumoral breast epithelial
cells with tunicamycin attenuates SOCE. Meanwhile, tunicamycin was without effect on SOCE
in luminal MCF7 and triple negative breast cancer (TNBC) MDA-MB-231 cells. Ca2+ imaging
experiments revealed that expression of the glycosylation-deficient Orai1 mutant (Orai1N223A)
did not alter SOCE in MCF10A, MCF7 and MDA-MB-231 cells. However, expression of the nonglycosylable STIM1 mutant (STIM1N131/171Q) significantly attenuated SOCE in MCF10A cells but
was without effect in SOCE in MCF7 and MDA-MB-231 cells. In non-tumoral cells impairment of
STIM1 N-linked glycosylation attenuated thapsigargin (TG)-induced caspase-3 activation while in
breast cancer cells, which exhibit a smaller caspase-3 activity in response to TG, expression of the
non-glycosylable STIM1 mutant (STIM1N131/171Q) was without effect on TG-evoked caspase-3
activation. Summarizing, STIM1 N-linked glycosylation is essential for full SOCE activation in
non-tumoral breast epithelial cells; by contrast, SOCE in breast cancer MCF7 and MDA-MB-231 cells
is insensitive to Orai1 and STIM1 N-linked glycosylation, and this event might participate in the
development of apoptosis resistance. | es |
dc.format | application/pdf | es |
dc.format.extent | 18 p. | es |
dc.language.iso | eng | es |
dc.publisher | MDPI | es |
dc.relation.ispartof | CANCERS, 15 (1), 203. | |
dc.rights | Atribución 4.0 Internacional | * |
dc.rights.uri | http://creativecommons.org/licenses/by/4.0/ | * |
dc.subject | Orai1 | es |
dc.subject | STIM1 | es |
dc.subject | Glycosylation | es |
dc.subject | Ca2+ entry | es |
dc.subject | Breast cancer cells | es |
dc.subject | Posttranslational modifications | es |
dc.subject | Store-operated Ca2+ entry | es |
dc.title | Store-operated calcium entry in breast cancer cells is insensitive to Orai1 and STIM1 N-linked glycosylation | 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.projectID | PID2019-104084GB-C21/AEI/ 10.13039/501100011033 | es |
dc.relation.projectID | PID2019-104084GB-C22/AEI/10.13039/501100011033 | es |
dc.relation.publisherversion | https://www.mdpi.com/2072-6694/15/1/203 | es |
dc.identifier.doi | 10.3390/cancers15010203 | es |
dc.journaltitle | CANCERS | es |
dc.publication.volumen | 15 | es |
dc.publication.issue | 1 | es |
dc.publication.initialPage | 203 | es |
dc.contributor.funder | Agencia Estatal de Investigación | es |