biostudies-literatureSinha STorey Pines Foundation, La JollaPadres Pedal the CauseUnited States National Institutes of HealthTorrey Pines FoundationNCI NIH HHSW.M. Keck FoundationNIH HHSUnited States National Institute of Healthe170953https://www.ebi.ac.uk/biostudies/studies/S-EPMC11645149biostudies-literatureUnknown134(24)Estrogen receptor-positive (ER+) breast cancer commonly disseminates to bone marrow, where interactions with mesenchymal stromal cells (MSCs) shape disease trajectory. We modeled these interactions with tumor-MSC co-cultures and used an integrated transcriptome-proteome-network-analyses workflow to identify a comprehensive catalog of contact-induced changes. Conditioned media from MSCs failed to recapitulate genes and proteins, some borrowed and others tumor-intrinsic, induced in cancer cells by direct contact. Protein-protein interaction networks revealed the rich connectome between "borrowed" and "intrinsic" components. Bioinformatics prioritized one of the borrowed components, CCDC88A/GIV, a multi-modular metastasis-related protein that has recently been implicated in driving a hallmarkThe Journal of clinical investigationBreast cancers that disseminate to bone marrow acquire aggressive phenotypes through CX43-related tumor-stroma tunnels.PMC11645149No fund numberR01 CA238042#PTC2021R33 CA225549P30 CA046592R01 CA238023R01 CA160911R37 CA222563R01 CA100768S10 OD026929R01CA238042,R01CA100768,R01CA160911,R50CA221807,U01CA210152,R01CA238023,R33CA225549,R37CA222563U01 CA210152994854R50 CA221807Masotti MLuker GDBuschhaus JMSinha SFarfel APCallow BWLuker KEGhosh PRoy SEspinoza CRRajendran SChen SfalseBreast cancers that disseminate to bone marrow acquire aggressive phenotypes through CX43-related tumor-stroma tunnels.Estrogen receptor-positive (ER+) breast cancer commonly disseminates to bone marrow, where interactions with mesenchymal stromal cells (MSCs) shape disease trajectory. We modeled these interactions with tumor-MSC co-cultures and used an integrated transcriptome-proteome-network-analyses workflow to identify a comprehensive catalog of contact-induced changes. Conditioned media from MSCs failed to recapitulate genes and proteins, some borrowed and others tumor-intrinsic, induced in cancer cells by direct contact. Protein-protein interaction networks revealed the rich connectome between "borrowed" and "intrinsic" components. Bioinformatics prioritized one of the borrowed components, CCDC88A/GIV, a multi-modular metastasis-related protein that has recently been implicated in driving a hallmark2024-01-01T00:00:00Z2024 Oct2026-07-15T08:11:17.314Z2025-04-04T01:54:36.303ZS-EPMC116451493948048810.1172/JCI170953