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PXD023224-2

PXD023224 is an original dataset announced via ProteomeXchange.

Dataset Summary
TitlePI3K-AKT pathway and cell-cell contact regulates maspin nuclear localization
DescriptionBackground: Maspin (SERPINB5) is a potential tumor suppressor gene with pleiotropic biological activities, including regulation of cell proliferation, death, adhesion, migration and gene expression. Several studies indicate that nuclear localization is essential for maspin tumor suppression activity. We have previously shown that the EGFR activation leads to maspin nuclear localization in MCF-10A cells. The present study investigated which EGFR downstream signaling molecules are involved in maspin nuclear localization and explored a possible role of cell-cell contact in this process. Methods: MCF-10A cells were treated with pharmacological inhibitors against EGFR downstream pathways followed by EGF treatment. Maspin subcellular localization was determined by immunofluorescence. To investigate the role of cell-cell contact these cells were either treated with chelating agents or plated on different cell densities. Maspin and E-cadherin subcellular localization was determined by immunofluorescence. In addition, proteomic and interactome analyses were conducted in order to identify molecular partners which interact with maspin in EGF-treated cells only. Results: EGFR activation regulates cell behavior via de extracellular signal–related kinase (ERK)/MAP kinase, phosphatidyl-inositol-3 (PI 3) kinase- AKT and Jak-STAT pathways. Using pharmacological inhibitors against key components of these signaling pathways we found that PI3K-AKT and Jak-STAT, but not MAP kinase pathway, regulate EGF-induced maspin nuclear accumulation in MCF-10A cells. Interestingly, we observed that maspin is predominantly nuclear in sparse cell culture, but it is redistributed to the cytoplasm in confluent cells even in the presence of EGF. Proteomic and interactome results suggest a role of maspin on post-transcriptional and translation regulation, protein folding and cell-cell adhesion.Conclusions: Maspin nuclear accumulation is determined by an interplay between EGFR (via PI3K-AKT and Jak-STAT pathways) and cell-to-cell contact.
HostingRepositoryPRIDE
AnnounceDate2024-10-22
AnnouncementXMLSubmission_2024-10-22_05:29:14.744.xml
DigitalObjectIdentifier
ReviewLevelPeer-reviewed dataset
DatasetOriginOriginal dataset
RepositorySupportUnsupported dataset by repository
PrimarySubmitterJulia Cunha
SpeciesList scientific name: Homo sapiens (Human); NCBI TaxID: 9606;
ModificationListNo PTMs are included in the dataset
InstrumentLTQ Orbitrap Velos
Dataset History
RevisionDatetimeStatusChangeLog Entry
02020-12-18 05:48:45ID requested
12021-09-09 15:18:40announced
22024-10-22 05:29:16announced2024-10-22: Updated project metadata.
Publication List
Longhi MT, Silva LE, Pereira M, Magalh, ã, es M, Reina J, Vitorino FNL, Gumbiner BM, da Cunha JPC, Cella N, PI3K-AKT, JAK2-STAT3 pathways and cell-cell contact regulate maspin subcellular localization. Cell Commun Signal, 19(1):86(2021) [pubmed]
10.1186/s12964-021-00758-3;
Keyword List
submitter keyword: cell-to-cell contact, Jak-STAT,maspin, EGFR, PI3K-AKT
Contact List
Nathalie Cella
contact affiliationDepartment of Cell and Developmental Biology, Institute of Biomedical Sciences, University of São Paulo, Av. Prof. Lineu Prestes, 1524, SP 05508-000, BR
contact emailncella@usp.br
lab head
Julia Cunha
contact affiliationLCC
contact emailjulia.cunha@butantan.gov.br
dataset submitter
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