Loss of myeloid‐specific lamin A/C drives lung metastasis through Gfi‐1 and C/EBPε‐mediated granulocytic differentiation

The immune‐suppressive tumor microenvironment promotes metastatic spread and outgrowth. One of the major contributors is tumor‐associated myeloid cells. However, the molecular mechanisms regulating their differentiation and function are not well understood. Here we report lamin A/C, a nuclear lamina...

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Veröffentlicht in:	Molecular carcinogenesis 2020-07, Vol.59 (7), p.679-690
Hauptverfasser:	Ishii, Hiroki, Park, Woo‐Yong, So, Jaeyoung, Kuhn, Skyler, Koparde, Vishal N., Pang, Yanli, Greten, Tim F., Hollander, M. Christine, Yang, Li
Format:	Artikel
Sprache:	eng
Schlagworte:	Animal models Animals Breast cancer CCAAT-Enhancer-Binding Proteins - genetics CD11b antigen Cell Differentiation - genetics Cells, Cultured Chemokines Chemokines - genetics Chromatin remodeling Disease Models, Animal Female Granulocytes - pathology granulocytic differentiation Humans immunosuppression Inflammation Inflammation - genetics Inflammation - pathology lamin A/C Lamin Type A - genetics Leukocytes, Mononuclear - pathology Lung cancer Lung Neoplasms - genetics Lung Neoplasms - pathology Metastases Metastasis Mice Mice, Inbred BALB C Mice, Inbred C57BL Mice, Knockout Molecular modelling Myeloid cells Myeloid Cells - pathology Neoplasm Metastasis - genetics Neoplasm Metastasis - pathology Peripheral blood Proto-Oncogene Proteins - genetics Repressor Proteins - genetics Transcription factors Triple Negative Breast Neoplasms - genetics Triple Negative Breast Neoplasms - pathology Tumor Microenvironment - genetics Up-Regulation - genetics
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