JunD enhances miR-29b levels transcriptionally and posttranscriptionally to inhibit proliferation of intestinal epithelial cells

Through its actions as component of the activating protein-1 (AP-1) transcription factor, JunD potently represses cell proliferation. Here we report a novel function of JunD in the regulation of microRNA expression in intestinal epithelial cells (IECs). Ectopically expressed JunD specifically increa...

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Published in	American Journal of Physiology: Cell Physiology Vol. 308; no. 10; pp. C813 - C824
Main Authors	Zou, Tongtong, Rao, Jaladanki N, Liu, Lan, Xiao, Lan, Chung, Hee Kyoung, Li, Yanwu, Chen, Gang, Gorospe, Myriam, Wang, Jian-Ying
Format	Journal Article
Language	English
Published	United States American Physiological Society 15.05.2015
Series	Cell Signaling: Proteins, Pathways and Mechanisms
Subjects	Animals Binding sites Call for Papers Cell Line Cell Proliferation Cells Epithelial Cells - cytology Epithelial Cells - metabolism Epithelium Homeostasis Humans Intestines - metabolism MicroRNAs - metabolism Mutation Protein Biosynthesis Protein expression Proto-Oncogene Proteins c-jun - metabolism Rats Transcription, Genetic - physiology microRNAs intestinal epithelial cells cell proliferation transcriptional factors transcriptional regulation
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Abstract	Through its actions as component of the activating protein-1 (AP-1) transcription factor, JunD potently represses cell proliferation. Here we report a novel function of JunD in the regulation of microRNA expression in intestinal epithelial cells (IECs). Ectopically expressed JunD specifically increased the expression of primary and mature forms of miR-29b, whereas JunD silencing inhibited miR-29b expression. JunD directly interacted with the miR-29b1 promoter via AP-1-binding sites, whereas mutation of AP-1 sites from the miR-29b1 promoter prevented JunD-mediated transcriptional activation of the miR-29b1 gene. JunD also enhanced formation of the Drosha microprocessor complex, thus further promoting miR-29b biogenesis. Cellular polyamines were found to regulate miR-29b expression by altering JunD abundance, since the increase in miR-29b expression levels in polyamine-deficient cells was abolished by JunD silencing. In addition, miR-29b silencing prevented JunD-induced repression of IEC proliferation. Our findings indicate that JunD activates miR-29b by enhancing its transcription and processing, which contribute to the inhibitory effect of JunD on IEC growth and maintenance of gut epithelium homeostasis.
AbstractList	Through its actions as component of the activating protein-1 (AP-1) transcription factor, JunD potently represses cell proliferation. Here we report a novel function of JunD in the regulation of microRNA expression in intestinal epithelial cells (IECs). Ectopically expressed JunD specifically increased the expression of primary and mature forms of miR-29b, whereas JunD silencing inhibited miR-29b expression. JunD directly interacted with the miR-29b1 promoter via AP-1-binding sites, whereas mutation of AP-1 sites from the miR-29b1 promoter prevented JunD-mediated transcriptional activation of the miR-29b1 gene. JunD also enhanced formation of the Drosha microprocessor complex, thus further promoting miR-29b biogenesis. Cellular polyamines were found to regulate miR-29b expression by altering JunD abundance, since the increase in miR-29b expression levels in polyamine-deficient cells was abolished by JunD silencing. In addition, miR-29b silencing prevented JunD-induced repression of IEC proliferation. Our findings indicate that JunD activates miR-29b by enhancing its transcription and processing, which contribute to the inhibitory effect of JunD on IEC growth and maintenance of gut epithelium homeostasis.
Author	Chung, Hee Kyoung Xiao, Lan Wang, Jian-Ying Chen, Gang Gorospe, Myriam Liu, Lan Zou, Tongtong Rao, Jaladanki N Li, Yanwu
Author_xml	– sequence: 1 givenname: Tongtong surname: Zou fullname: Zou, Tongtong organization: Cell Biology Group, Department of Surgery, University of Maryland School of Medicine, Baltimore, Maryland; Baltimore Veterans Affairs Medical Center, Baltimore, Maryland – sequence: 2 givenname: Jaladanki N surname: Rao fullname: Rao, Jaladanki N organization: Cell Biology Group, Department of Surgery, University of Maryland School of Medicine, Baltimore, Maryland; Baltimore Veterans Affairs Medical Center, Baltimore, Maryland – sequence: 3 givenname: Lan surname: Liu fullname: Liu, Lan organization: Cell Biology Group, Department of Surgery, University of Maryland School of Medicine, Baltimore, Maryland; Baltimore Veterans Affairs Medical Center, Baltimore, Maryland – sequence: 4 givenname: Lan surname: Xiao fullname: Xiao, Lan organization: Cell Biology Group, Department of Surgery, University of Maryland School of Medicine, Baltimore, Maryland; Baltimore Veterans Affairs Medical Center, Baltimore, Maryland – sequence: 5 givenname: Hee Kyoung surname: Chung fullname: Chung, Hee Kyoung organization: Cell Biology Group, Department of Surgery, University of Maryland School of Medicine, Baltimore, Maryland; Baltimore Veterans Affairs Medical Center, Baltimore, Maryland – sequence: 6 givenname: Yanwu surname: Li fullname: Li, Yanwu organization: Cell Biology Group, Department of Surgery, University of Maryland School of Medicine, Baltimore, Maryland; Baltimore Veterans Affairs Medical Center, Baltimore, Maryland – sequence: 7 givenname: Gang surname: Chen fullname: Chen, Gang organization: Cell Biology Group, Department of Surgery, University of Maryland School of Medicine, Baltimore, Maryland; Baltimore Veterans Affairs Medical Center, Baltimore, Maryland – sequence: 8 givenname: Myriam surname: Gorospe fullname: Gorospe, Myriam organization: Laboratory of Genetics and Genomics, National Institute on Aging-Intramural Research Program, National Institutes of Health, Baltimore, Maryland; and – sequence: 9 givenname: Jian-Ying surname: Wang fullname: Wang, Jian-Ying email: jwang@smail.umaryland.edu organization: Cell Biology Group, Department of Surgery, University of Maryland School of Medicine, Baltimore, Maryland; Baltimore Veterans Affairs Medical Center, Baltimore, Maryland; Department of Pathology, University of Maryland School of Medicine, Baltimore, Maryland jwang@smail.umaryland.edu
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Snippet	Through its actions as component of the activating protein-1 (AP-1) transcription factor, JunD potently represses cell proliferation. Here we report a novel...
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SubjectTerms	Animals Binding sites Call for Papers Cell Line Cell Proliferation Cells Epithelial Cells - cytology Epithelial Cells - metabolism Epithelium Homeostasis Humans Intestines - metabolism MicroRNAs - metabolism Mutation Protein Biosynthesis Protein expression Proto-Oncogene Proteins c-jun - metabolism Rats Transcription, Genetic - physiology
Title	JunD enhances miR-29b levels transcriptionally and posttranscriptionally to inhibit proliferation of intestinal epithelial cells
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