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PXD046265

PXD046265 is an original dataset announced via ProteomeXchange.

Dataset Summary
Title2D-PAGE coupled with nLC-MS/MS-based identification of differentialy expressed proteins and tumorigenic pathways in MCF7 breast cancer cell line transfected for JTB protein silencing
DescriptionIdentification of new cancer-associated genes/proteins, characterization of their expression vari-ation, the interactomics-based assessment of differentially expressed genes/proteins (DEGs/DEPs), and understanding the tumorigenic pathways and biological processes involved in BC genesis and progression are necessary and possible by rapid and recent advances in bioin-formatics and molecular profiling strategies. Taking into account the opinion of other authors, as well as based on our own team’s in vitro studies, we sustain that JTB protein might be consid-ered as a tumor biomarker for BC and should be studied as a target for BC therapy. In this study we have identified the differentially expressed proteins (DEPs), carcinogenic pathways and bio-logical processes associated with JTB silencing, using 2D-PAGE coupled with nano-liquid chro-matography tandem mass spectrometry (nLC-MS/MS) proteomics applied to MCF7 breast cancer cell line, for complementing and completing our previous results based on SDS-PAGE, as well as in-solution proteomics of MCF7 cells transfected for JTB downregulation. The functions of significant DEPs have been analysed using GSEA and KEGG analysis. Almost all DEPs exert protumorigenic effects in JTBlow condition, sustaining the tumor suppressive function of JTB. Thus, the identified DEPs are involved in several signaling and metabolic pathways that exert protumorigenic roles: EMT, ERK/MAPK, PI3K/AKT, Wnt/β-catenin, mTOR, C-MYC, NF-κB, IFN-γ and IFN-α response, UPR, and glycolysis/gluconeogenesis. These pathways sustain cancer cell growth, adhesion, survival, proliferation, invasion, metastasis, resistance to apoptosis, cytoskeleton reorganization, maintenance of stemness, metabolic reprogramming, survival into a hostile environment, and a poor clinical outocome. In conclusion, JTB silencing might increase the neoplastic phenotype and behavior of MCF7 BC cell line.
HostingRepositoryPRIDE
AnnounceDate2024-01-26
AnnouncementXMLSubmission_2024-01-26_07:29:04.893.xml
DigitalObjectIdentifier
ReviewLevelPeer-reviewed dataset
DatasetOriginOriginal dataset
RepositorySupportUnsupported dataset by repository
PrimarySubmitterDanielle Whitham
SpeciesList scientific name: Homo sapiens (Human); NCBI TaxID: 9606;
ModificationListmonohydroxylated residue; iodoacetamide derivatized residue
InstrumentXevo G2 Q-Tof
Dataset History
RevisionDatetimeStatusChangeLog Entry
02023-10-20 10:20:13ID requested
12024-01-26 07:29:06announced
Publication List
10.3390/molecules28227501;
Jayathirtha M, Jayaweera T, Whitham D, Sullivan I, Petre BA, Darie CC, Neagu AN, Two-Dimensional-PAGE Coupled with nLC-MS/MS-Based Identification of Differentially Expressed Proteins and Tumorigenic Pathways in MCF7 Breast Cancer Cells Transfected for JTB Protein Silencing. Molecules, 28(22):(2023) [pubmed]
Keyword List
submitter keyword: breast cancer (BC)
MCF7
JTB protein silencing
overexpressed JTB-interactome
downregulated JTB-interactome
tumorigenic pathways
Contact List
Anca-Narcia Neagu
contact affiliationLaboratory of Animal Histology, Faculty of Biology, “Alexandru Ioan Cuza” University of Iasi, Carol I Bvd. No. 22, Iasi 700505, Romania
contact emailaneagu@uaic.ro
lab head
Danielle Whitham
contact affiliationClarkson University
contact emailwhithad@clarkson.edu
dataset submitter
Full Dataset Link List
Dataset FTP location
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