{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Wang H"],"funding":["National Key R&amp;D Program of China","NSFC | National Outstanding Youth Science Fund Project of National Natural Science Foundation of China","National Natural Science Foundation of China","Tianjin Science and Technology Committee"],"pagination":["e149551"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC9433100"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["132(17)"],"pubmed_abstract":["The switch from anchorage-dependent to anchorage-independent growth is essential for epithelial metastasis. The underlying mechanism, however, is not fully understood. In this study, we identified growth factor independent-1 (GFI1), a transcription factor that drives the transition from adherent endothelial cells to suspended hematopoietic cells during hematopoiesis, as a critical regulator of anchorage independence in lung cancer cells. GFI1 elevated the numbers of circulating and lung-infiltrating tumor cells in xenograft models and predicted poor prognosis of patients with lung cancer. Mechanistically, GFI1 inhibited the expression of multiple adhesion molecules and facilitated substrate detachment. Concomitantly, GFI1 reconfigured the chromatin structure of the RASGRP2 gene and increas"],"journal":["The Journal of clinical investigation"],"pubmed_title":["Hematopoietic transcription factor GFI1 promotes anchorage independence by sustaining ERK activity in cancer cells."],"pmcid":["PMC9433100"],"funding_grant_id":["20JCZDJC00110","2018YFC1313000","81872350","2018YFC1313002","17JCYBJC27600","8217113342","81773034","81602018","18JCZDJC99100","81825017"],"pubmed_authors":["Zhang W","Liu Z","Zhang Z","Xiao Z","Ma Z","Wang H","Lin Z","Wang X","Nian Z","Liu W","Yan F"],"additional_accession":[]},"is_claimable":false,"name":"Hematopoietic transcription factor GFI1 promotes anchorage independence by sustaining ERK activity in cancer cells.","description":"The switch from anchorage-dependent to anchorage-independent growth is essential for epithelial metastasis. The underlying mechanism, however, is not fully understood. In this study, we identified growth factor independent-1 (GFI1), a transcription factor that drives the transition from adherent endothelial cells to suspended hematopoietic cells during hematopoiesis, as a critical regulator of anchorage independence in lung cancer cells. GFI1 elevated the numbers of circulating and lung-infiltrating tumor cells in xenograft models and predicted poor prognosis of patients with lung cancer. Mechanistically, GFI1 inhibited the expression of multiple adhesion molecules and facilitated substrate detachment. Concomitantly, GFI1 reconfigured the chromatin structure of the RASGRP2 gene and increas","dates":{"release":"2022-01-01T00:00:00Z","publication":"2022 Sep","modification":"2026-05-10T05:13:29.243Z","creation":"2025-02-19T04:02:59.812Z"},"accession":"S-EPMC9433100","cross_references":{"pubmed":["35819844"],"doi":["10.1172/JCI149551"]}}