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Keratin-dependent regulation of Aire and gene expression in skin tumor keratinocytes
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Keratin-dependent regulation of Aire and gene expression in skin tumor keratinocytes
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Journal Article
Keratin-dependent regulation of Aire and gene expression in skin tumor keratinocytes
2015
Overview
Pierre Coulombe and colleagues show that the autoimmune regulator Aire is induced in tumor keratinocytes in a keratin 17 (K17)-dependent manner and promotes skin tumorigenesis in mice. They further show that K17 and Aire colocalize in the nucleus and bind a subset of proinflammatory genes, providing a molecular explanation for the K17-dependent amplification of inflammatory responses in diseased epithelia.
Expression of the intermediate filament protein keratin 17 (K17) is robustly upregulated in inflammatory skin diseases and in many tumors originating in stratified and pseudostratified epithelia
1
,
2
,
3
. We report that autoimmune regulator (Aire), a transcriptional regulator, is inducibly expressed in human and mouse tumor keratinocytes in a K17-dependent manner and is required for timely onset of
Gli2
-induced skin tumorigenesis in mice. The induction of
Aire
mRNA in keratinocytes depends on a functional interaction between K17 and the heterogeneous nuclear ribonucleoprotein hnRNP K
4
. Further, K17 colocalizes with Aire protein in the nucleus of tumor-prone keratinocytes, and each factor is bound to a specific promoter region featuring an NF-κB consensus sequence in a relevant subset of K17- and Aire-dependent proinflammatory genes. These findings provide radically new insight into keratin intermediate filament and Aire function, along with a molecular basis for the K17-dependent amplification of inflammatory and immune responses in diseased epithelia.
Publisher
Nature Publishing Group US,Nature Publishing Group
Subject
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/ 13/109
/ 13/21
/ 13/31
/ 13/51
/ 13/89
/ 14/19
/ 14/32
/ 14/35
/ 14/63
/ 38/39
/ 38/77
/ 631/337
/ 64/60
/ 82/29
/ Animal Genetics and Genomics
/ Animals
/ Genes
/ Humans
/ Keratin
/ letter
/ Reverse Transcriptase Polymerase Chain Reaction
/ Skin
/ Transcription Factors - genetics
/ Transcription Factors - metabolism
/ Tumors
