{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Ratze MAK"],"funding":["National Centre for the Replacement, Refinement and Reduction of Animals in Research","Medical Research Council","Dutch Research Council (NWO)"],"pagination":["2932-2944"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC9122823"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["41(21)"],"pubmed_abstract":["Invasive lobular breast carcinoma (ILC) is characterized by proliferative indolence and long-term latency relapses. This study aimed to identify how disseminating ILC cells control the balance between quiescence and cell cycle re-entry. In the absence of anchorage, ILC cells undergo a sustained cell cycle arrest in G0/G1 while maintaining viability. From the genes that are upregulated in anchorage independent ILC cells, we selected Inhibitor of DNA binding 2 (Id2), a mediator of cell cycle progression. Using loss-of-function experiments, we demonstrate that Id2 is essential for anchorage independent survival (anoikis resistance) in vitro and lung colonization in mice. Importantly, we find that under anchorage independent conditions, E-cadherin loss promotes expression of Id2 in multiple mo"],"journal":["Oncogene"],"pubmed_title":["Loss of E-cadherin leads to Id2-dependent inhibition of cell cycle progression in metastatic lobular breast cancer."],"pmcid":["PMC9122823"],"funding_grant_id":["NC/P001262/1","016.096.318"],"pubmed_authors":["Sijnesael T","Bassey-Archibong B","Enserink L","O'Leary L","Bakker ERM","Richard F","Derksen PWB","Viciano I","Roca-Cusachs P","Jaksani S","Isacke CM","Visser D","van Diest PJ","Desmedt C","van de Ven R","Ratze MAK","Tutt A","Daniel JM","Koorman T","Fitzpatrick A"],"additional_accession":[]},"is_claimable":false,"name":"Loss of E-cadherin leads to Id2-dependent inhibition of cell cycle progression in metastatic lobular breast cancer.","description":"Invasive lobular breast carcinoma (ILC) is characterized by proliferative indolence and long-term latency relapses. This study aimed to identify how disseminating ILC cells control the balance between quiescence and cell cycle re-entry. In the absence of anchorage, ILC cells undergo a sustained cell cycle arrest in G0/G1 while maintaining viability. From the genes that are upregulated in anchorage independent ILC cells, we selected Inhibitor of DNA binding 2 (Id2), a mediator of cell cycle progression. Using loss-of-function experiments, we demonstrate that Id2 is essential for anchorage independent survival (anoikis resistance) in vitro and lung colonization in mice. Importantly, we find that under anchorage independent conditions, E-cadherin loss promotes expression of Id2 in multiple mo","dates":{"release":"2022-01-01T00:00:00Z","publication":"2022 May","modification":"2025-04-04T07:34:19.781Z","creation":"2025-02-19T01:24:00.292Z"},"accession":"S-EPMC9122823","cross_references":{"pubmed":["35437308"],"doi":["10.1038/s41388-022-02314-w"]}}