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Nuclear Janus-activated kinase 2/nuclear factor 1-C2 suppresses tumorigenesis and epithelial-to-mesenchymal transition by repressing Forkhead box F1.

Journal article
Authors Jeanette Nilsson
Khalil Helou
Anikó Kovács
Pär-Ola Bendahl
Gunnar Bjursell
Mårten Fernö
Peter Carlsson
Marie Kannius-Janson
Published in Cancer research
Volume 70
Issue 5
Pages 2020-2029
ISSN 1538-7445
Publication year 2010
Published at Department of Cell and Molecular Biology
Institute of Clinical Sciences, Department of Oncology
Department of Cell and Molecular Biology, Molecular Biology
Pages 2020-2029
Language en
Keywords Animals, Breast Neoplasms, genetics, metabolism, pathology, Cell Adhesion, physiology, Cell Growth Processes, physiology, Cell Line, Tumor, Cell Movement, physiology, Epithelial Cells, pathology, Female, Forkhead Transcription Factors, antagonists & inhibitors, biosynthesis, genetics, metabolism, Humans, Janus Kinase 2, metabolism, Mesoderm, pathology, Mice, Mice, Inbred BALB C, Mice, Nude, NFI Transcription Factors, metabolism, Promoter Regions, Genetic
Subject categories Cancer and Oncology


Progression to metastasis is the proximal cause of most cancer-related mortality. Yet much remains to be understood about what determines the spread of tumor cells. This paper describes a novel pathway in breast cancer that regulates epithelial-to-mesenchymal transition (EMT), motility, and invasiveness. We identify two transcription factors, nuclear factor 1-C2 (NF1-C2) and Forkhead box F1 (FoxF1), downstream of prolactin/nuclear Janus-activated kinase 2, with opposite effects on these processes. We show that NF1-C2 is lost during mammary tumor progression and is almost invariably absent from lymph node metastases. NF1-C2 levels in primary tumors correlate with better patient survival. Manipulation of NF1-C2 levels by expression of a stabilized version or using small interfering RNA showed that NF1-C2 counteracts EMT, motility, invasiveness, and tumor growth. FoxF1 was found to be a direct repressed target of NF1-C2. We provide the first evidence for a role of FoxF1 in cancer and in the regulation of EMT in cells of epithelial origin. Overexpression of FoxF1 was associated with a mesenchymal phenotype, increased invasiveness in vitro, and enhanced growth of breast carcinoma xenografts in nude mice. The relevance of these findings is strengthened by the correlation between FoxF1 expression and a mesenchymal phenoype in breast cancer cell isolates, consistent with the interpretation that FoxF1 promotes invasion and metastasis.

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