Psoriasin: A Novel Chemotactic Protein

Jinquan, Tan; Vorum, Henrik; Larsen, Christian Grónhøj; Madsen, Peder; Rasmussen, Hanne H.; Gesser, Borbala; Etzerodt, Michael; Honoré, Bent; Celis, Julio E.; Thestrup‐Pedersen, Kristian

doi:10.1111/1523-1747.ep12294284

Cited by 217 publications

(177 citation statements)

References 40 publications

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“…6). S100 family members have also been demonstrated to be involved in the response to infection (51)(52)(53). In addition to S100A7, S100A8, and S100A9, which were previously reported to be up-regulated by IL-22 (13,14), we found that S100A12 and S100A15 were strongly induced by the IL-20 subfamily of cytokines (supplemental Table I and Fig.…”

Section: Unique Gene Signatures Induced By Il-20 Subfamily Cytokines supporting

confidence: 63%

“…S100 family proteins were some of the most highly up-regulated genes in our microarrays and as determined by quantitative RT-PCR. Proteins of this family, whose genes are found in the epidermal differentiation complex, are calcium-binding proteins that are associated with inflammation, some of which have been shown to have chemotactic and direct antimicrobial activities (51)(52)(53). Other genes induced by the IL-20 subfamily cytokines and also in psoriatic skin include chemokines, angiogenic factors, tissue kallikreins, and ␤-defensins (38,48,49,71).…”

Section: Discussionmentioning

confidence: 99%

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The Effects of IL-20 Subfamily Cytokines on Reconstituted Human Epidermis Suggest Potential Roles in Cutaneous Innate Defense and Pathogenic Adaptive Immunity in Psoriasis

Susan

Valdez²,

Wu³

et al. 2007

The Journal of Immunology

440

256

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IL-19, IL-20, IL-22, IL-24, and IL-26 are members of the IL-10 family of cytokines that have been shown to be up-regulated in psoriatic skin. Contrary to IL-10, these cytokines signal using receptor complex R1 subunits that are preferentially expressed on cells of epithelial origin; thus, we henceforth refer to them as the IL-20 subfamily cytokines. In this study, we show that primary human keratinocytes (KCs) express receptors for these cytokines and that IL-19, IL-20, IL-22, and IL-24 induce acanthosis in reconstituted human epidermis (RHE) in a dose-dependent manner. These cytokines also induce expression of the psoriasisassociated protein S100A7 and keratin 16 in RHE and cause persistent activation of Stat3 with nuclear localization. IL-22 had the most pronounced effects on KC proliferation and on the differentiation of KCs in RHE, inducing a decrease in the granular cell layer (hypogranulosis). Furthermore, gene expression analysis performed on cultured RHE treated with these cytokines showed that IL-19, IL-20, IL-22, and IL-24 regulate many of these same genes to variable degrees, inducing a gene expression profile consistent with inflammatory responses, wound healing re-epithelialization, and altered differentiation. Many of these genes have also been found to be up-regulated in psoriatic skin, including several chemokines, ␤-defensins, S100 family proteins, and kallikreins. These results confirm that IL-20 subfamily cytokines are important regulators of epidermal KC biology with potentially pivotal roles in the immunopathology of psoriasis.

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Section: Unique Gene Signatures Induced By Il-20 Subfamily Cytokines supporting

confidence: 63%

Section: Discussionmentioning

confidence: 99%

The Effects of IL-20 Subfamily Cytokines on Reconstituted Human Epidermis Suggest Potential Roles in Cutaneous Innate Defense and Pathogenic Adaptive Immunity in Psoriasis

Susan

Valdez²,

Wu³

et al. 2007

The Journal of Immunology

440

256

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“…Discussion S100A7 is commonly upregulated in breast cancer, most frequently in ductal carcinoma in situ with a high grade, ER-negative phenotype (Emberley et al, 2004a, b). The frequent association of inflammation with this tumor phenotype supports the view that S100A7 may be a chemotactic factor for inflammatory cells (Jinquan et al, 1996;Wolf et al, 2008), although it is also possible that inflammation may precede and stimulate S100A7. We have shown here that two IL-6 family cytokines, OSM and IL-6, regulate S100A7 in breast cell lines via (in MCF7 cells) PI3K, ERK1/2 and STAT3 signaling.…”

Section: Inflammatory Cytokines Induce S100a7 Expression In Breast Cellssupporting

confidence: 56%

S100A7 (psoriasin) is induced by the proinflammatory cytokines oncostatin-M and interleukin-6 in human breast cancer

West

Watson

2010

Oncogene

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S100A7 promotes aggressive features in breast cancer, although regulation of its expression is poorly understood. As S100A7 associates with inflammation in skin and breast tissue, we hypothesized that inflammatory cytokines may regulate S100A7 in breast cancer. We therefore examined the effects of several cytokines, among which oncostatin-M (OSM) and the related cytokine, interleukin (IL)-6, showed the most significant effects on S100A7 expression in breast tumor cells in vitro. Both cytokines consistently induced S100A7 expression in three cell lines (MCF7, T47D and MDA-MB-468) in a dose-and time-dependent manner. Induction of S100A7 was inhibited by blockade of STAT3, phosphatidylinositol 3 kinase (PI3K) and ERK1/2 signaling and small interference RNA (siRNA)-mediated knockdown of S100A7 eliminated the promigratory effects of OSM treatment. S100A7 mRNA levels in a case-control cohort of breast tumors (n ¼ 20) were significantly associated with expression of the OSM receptor b (OSMRb) chain (P ¼ 0.0098). This association was confirmed using publicly available microarray data from an independent breast tumor cohort (n ¼ 201, P ¼ 0.0005) and a correlation between S100A7 and poor patient survival was observed specifically in cases with high OSMRb expression (HR ¼ 2.35; P ¼ 0.0396; n ¼ 85). We conclude that inflammatory cytokines can regulate S100A7 expression and that S100A7 may mediate some of their effects in breast cancer.

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“…In fact, S100A7 has been identified in unbiased studies of mRNA and protein expression as amongst the most highly expressed genes in certain subsets of breast tumours (Leygue et al 1996, Al-Haddad et al 1999, Emberley et al 2003. Some of its effects are mediated by intracellular interaction with JAB1 (Emberley et al 2003, but S100A7 is also secreted and has chemotactic effects on inflammatory cells (Jinquan et al 1996). Indeed, the mouse S100A7 homologue recruits tumour-associated macrophages in a murine orthotopic breast cancer model (Nasser et al 2012).…”

Section: Cd68mentioning

confidence: 99%

Intratumoural inflammation and endocrine resistance in breast cancer

Murray¹,

West²,

Murphy³

et al. 2014

Endocrine-Related Cancer

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It is becoming clear that inflammation-associated mechanisms can affect progression of breast cancer and modulate responses to treatment. Estrogen receptor alpha (ERa (ESR1)) is the principal biomarker and therapeutic target for endocrine therapies in breast cancer. Over 70% of patients are ESR1-positive at diagnosis and are candidates for endocrine therapy. However, ESR1-positive tumours can become resistant to endocrine therapy. Multiple mechanisms of endocrine resistance have been proposed, including suppression of ESR1. This review discusses the relationship between intratumoural inflammation and endocrine resistance with a particular focus on inflammation-mediated suppression of ESR1.

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Psoriasin: A Novel Chemotactic Protein

Cited by 217 publications

References 40 publications

The Effects of IL-20 Subfamily Cytokines on Reconstituted Human Epidermis Suggest Potential Roles in Cutaneous Innate Defense and Pathogenic Adaptive Immunity in Psoriasis

The Effects of IL-20 Subfamily Cytokines on Reconstituted Human Epidermis Suggest Potential Roles in Cutaneous Innate Defense and Pathogenic Adaptive Immunity in Psoriasis

S100A7 (psoriasin) is induced by the proinflammatory cytokines oncostatin-M and interleukin-6 in human breast cancer

Intratumoural inflammation and endocrine resistance in breast cancer

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