Hematopoietic transcription factor GFI1 promotes anchorage independence by sustaining ERK activity in cancer cells.

Szczegóły
Abstrakt

Tytuł:: Hematopoietic transcription factor GFI1 promotes anchorage independence by sustaining ERK activity in cancer cells.
Autorzy:: Wang H; State Key Laboratory of Experimental Hematology, Haihe Laboratory of Cell Ecosystem, The Province and Ministry Co-sponsored Collaborative Innovation Center for Medical Epigenetics, Key Laboratory of Immune Microenvironment and Disease of the Ministry of Education, Department of Immunology, School of Basic Medical Sciences, Tianjin Medical University, Tianjin, China.
Lin Z; State Key Laboratory of Experimental Hematology, Haihe Laboratory of Cell Ecosystem, The Province and Ministry Co-sponsored Collaborative Innovation Center for Medical Epigenetics, Key Laboratory of Immune Microenvironment and Disease of the Ministry of Education, Department of Immunology, School of Basic Medical Sciences, Tianjin Medical University, Tianjin, China.
Nian Z; State Key Laboratory of Experimental Hematology, Haihe Laboratory of Cell Ecosystem, The Province and Ministry Co-sponsored Collaborative Innovation Center for Medical Epigenetics, Key Laboratory of Immune Microenvironment and Disease of the Ministry of Education, Department of Immunology, School of Basic Medical Sciences, Tianjin Medical University, Tianjin, China.
Zhang W; State Key Laboratory of Experimental Hematology, Haihe Laboratory of Cell Ecosystem, The Province and Ministry Co-sponsored Collaborative Innovation Center for Medical Epigenetics, Key Laboratory of Immune Microenvironment and Disease of the Ministry of Education, Department of Immunology, School of Basic Medical Sciences, Tianjin Medical University, Tianjin, China.
Liu W; State Key Laboratory of Experimental Hematology, Haihe Laboratory of Cell Ecosystem, The Province and Ministry Co-sponsored Collaborative Innovation Center for Medical Epigenetics, Key Laboratory of Immune Microenvironment and Disease of the Ministry of Education, Department of Immunology, School of Basic Medical Sciences, Tianjin Medical University, Tianjin, China.
Yan F; State Key Laboratory of Experimental Hematology, Haihe Laboratory of Cell Ecosystem, The Province and Ministry Co-sponsored Collaborative Innovation Center for Medical Epigenetics, Key Laboratory of Immune Microenvironment and Disease of the Ministry of Education, Department of Immunology, School of Basic Medical Sciences, Tianjin Medical University, Tianjin, China.
Xiao Z; State Key Laboratory of Experimental Hematology, Haihe Laboratory of Cell Ecosystem, The Province and Ministry Co-sponsored Collaborative Innovation Center for Medical Epigenetics, Key Laboratory of Immune Microenvironment and Disease of the Ministry of Education, Department of Immunology, School of Basic Medical Sciences, Tianjin Medical University, Tianjin, China.; Department of Lung Cancer Center and.
Wang X; Department of Gastroenterology, Tianjin Medical University Cancer Institute and Hospital, Tianjin, China.
Zhang Z; Department of Lung Cancer Center and.
Ma Z; State Key Laboratory of Experimental Hematology, Haihe Laboratory of Cell Ecosystem, The Province and Ministry Co-sponsored Collaborative Innovation Center for Medical Epigenetics, Key Laboratory of Immune Microenvironment and Disease of the Ministry of Education, Department of Immunology, School of Basic Medical Sciences, Tianjin Medical University, Tianjin, China.
Liu Z; State Key Laboratory of Experimental Hematology, Haihe Laboratory of Cell Ecosystem, The Province and Ministry Co-sponsored Collaborative Innovation Center for Medical Epigenetics, Key Laboratory of Immune Microenvironment and Disease of the Ministry of Education, Department of Immunology, School of Basic Medical Sciences, Tianjin Medical University, Tianjin, China.; Department of Cell Biology, School of Basic Medical Sciences, Hangzhou Normal University, Hangzhou, China.; Collaborative Innovation Center for Cancer Personalized Medicine, Nanjing Medical University, Nanjing, China.
Źródło:: The Journal of clinical investigation [J Clin Invest] 2022 Sep 01; Vol. 132 (17).
Typ publikacji:: Journal Article; Research Support, Non-U.S. Gov't
Język:: English
Imprint Name(s):: Publication: 1999- : Ann Arbor, MI : American Society for Clinical Investigation
Original Publication: New Haven [etc.] American Society for Clinical Investigation.
MeSH Terms:: DNA-Binding Proteins*/genetics
DNA-Binding Proteins*/metabolism
Lung Neoplasms*/genetics
Transcription Factors*/genetics
Transcription Factors*/metabolism
Animals ; Endothelial Cells/metabolism ; Gene Expression Regulation ; Guanine Nucleotide Exchange Factors/genetics ; Hematopoiesis ; Humans
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Contributed Indexing:: Keywords: Apoptosis survival pathways; Cancer; Cell Biology; Cell migration/adhesion; Oncology
Substance Nomenclature:: 0 (DNA-Binding Proteins)
0 (GFI1 protein, human)
0 (Guanine Nucleotide Exchange Factors)
0 (RASGRP2 protein, human)
0 (Transcription Factors)
Entry Date(s):: Date Created: 20220712 Date Completed: 20220908 Latest Revision: 20221006
Update Code:: 20240105
PubMed Central ID:: PMC9433100
DOI:: 10.1172/JCI149551
PMID:: 35819844
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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 increased its expression, causing Rap1 activation and subsequent sustained ERK activation upon detachment, and this led to ERK signaling dependency in tumor cells. Our studies unveiled a mechanism by which carcinoma cells hijacked a hematopoietic factor to gain anchorage independence and suggested that the intervention of ERK signaling may suppress metastasis and improve the therapeutic outcome of patients with GFI1-positive lung cancer.

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