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FOXM1 is a critical driver of lung fibroblast activation and fibrogenesis
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FOXM1 is a critical driver of lung fibroblast activation and fibrogenesis
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Journal Article
FOXM1 is a critical driver of lung fibroblast activation and fibrogenesis
2018
Overview
While the transcription factor forkhead box M1 (FOXM1) is well known as a proto-oncogene, its potential role in lung fibroblast activation has never been explored. Here, we show that FOXM1 is more highly expressed in fibrotic than in normal lung fibroblasts in humans and mice. FOXM1 was required not only for cell proliferation in response to mitogens, but also for myofibroblast differentiation and apoptosis resistance elicited by TGF-β. The lipid mediator PGE2, acting via cAMP signaling, was identified as an endogenous negative regulator of FOXM1. Finally, genetic deletion of FOXM1 in fibroblasts or administration of the FOXM1 inhibitor Siomycin A in a therapeutic protocol attenuated bleomycin-induced pulmonary fibrosis. Our results identify FOXM1 as a driver of lung fibroblast activation and underscore the therapeutic potential of targeting FOXM1 for pulmonary fibrosis.
Publisher
American Society for Clinical Investigation
Subject
/ Cancer
/ Cell Proliferation - drug effects
/ Cell Proliferation - genetics
/ Female
/ Fibrosis
/ Forkhead Box Protein M1 - antagonists & inhibitors
/ Forkhead Box Protein M1 - genetics
/ Forkhead Box Protein M1 - metabolism
/ Forkhead transcription factors
/ Humans
/ Kinases
/ Lung
/ Lungs
/ Mice
/ Mitogens
/ Proteins
/ Pulmonary Fibrosis - chemically induced
/ Pulmonary Fibrosis - drug therapy
/ Pulmonary Fibrosis - genetics
