Psoriasin (S100A7) increases the expression of ROS and VEGF and acts through RAGE to promote endothelial cell proliferation

Shubbar, Emman; Vegfors, Jenny; Carlström, Maria; Petersson, Stina; Enerbäck, Charlotta

doi:10.1007/s10549-011-1920-5

Cited by 64 publications

(75 citation statements)

References 43 publications

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“…In pancreatic cancer, the expression of S100A4 and S100P was associated with drug resistence, differentiation, metastasis and clinical outcome and S100A11 and S100P, and possibly also S100A2 and S100A6 were related to the unfavorable outcome of the patients after surgical resection 61 . S100A7/psoriasin was highly expressed in high-grade ductal breast carcinoma in situ 62 , high-grade comedo ductal carcinoma in situ with higher risk of local recurrence 63 and in invasive estrogen receptor negative breast cancer 64 . Its expression was related to ductal hyperplasia, recruitment of tumor-associated macrophages, tumor growth, angiogenesis and metastasis.…”

Section: S100 Proteins and Cancermentioning

confidence: 99%

“…Tumor growth was inhib-ited by the downregulation of psoriasin by short hairpin RNA (shRNA) resulting in decreased expression of vascular endothelial growth factor (VEGF) (ref. 62 ). Invasion of breast cancer may be also stimulated by S100A8/A9 via RAGE-mediated epithelial-mesenchymal transition through NF-κB mediated stabilization of Snail.…”

Section: S100 Proteins and Cancermentioning

confidence: 99%

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HMGB1, S100 proteins and other RAGE ligands in cancer - markers, mediators and putative therapeutic targets

et al. 2016

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Background and Aims. Activation of RAGE due to its increased expression in cancer cells or its stimulation by multiple ligands (AGEs, HMGB1, S100 proteins, etc.) may contribute to the proliferation, invasiveness of tumor cells and formation of distant metastases and also to the resistance of cancer to treatment. RAGE ligands could thus become both useful markers of disease severity and its outcome and, a potential therapeutic target. Conclusions. Better understanding of the role of RAGE activation in different types of cancer may help to define the role of ligand/RAGE antagonists as promising cancer treatment.

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Section: S100 Proteins and Cancermentioning

confidence: 99%

Section: S100 Proteins and Cancermentioning

confidence: 99%

HMGB1, S100 proteins and other RAGE ligands in cancer - markers, mediators and putative therapeutic targets

et al. 2016

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“…Glyceraldehyde-3-phosphate dehydrogenase (GAPDH), β-actin and ribosomal protein, large, P0 (RPLP0) were used as the reference genes. The primers for psoriasin, VEGF, RAGE and GAPDH have been previously described [106][107][108][109][110]. The primers for the remaining target genes were designed using the Primer Express Software version 3.0.…”

Section: Quantitative Real-time Pcr (Qpcr)mentioning

confidence: 99%

“…Thus, psoriasin secreted from epithelial cells may interact with RAGE on the surface of endothelial cells, which may in turn induce angiogenesis. [110] Low levels of ROS induce proliferation of a variety of cells, among them the endothelial cells [131]. ROS also induces VEGF expression [132].…”

Section: Paper Imentioning

confidence: 99%

“…Altogether, these findings suggest that psoriasin induces proliferation of endothelial cells through the interaction with RAGE and increased levels of ROS. [110] ROS affects a wide range of cellular functions, from cell proliferation to cell death, depending on differences in the amount and duration of ROS production. Exposure of endothelial cells to low concentrations of H 2 O 2 stimulates cell proliferation and angiogenesis, whereas severe oxidative stress causes cell death [131,[134][135].…”

Section: Paper Imentioning

confidence: 99%

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Psoriasin For Better or for Worse in Sickness and in Health : The Role of Psoriasin in Angiogenesis and Differentation of Epithelial Cells

Vegfors¹

2014

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-I - ABSTRACTPsoriasin (S100A7), a member of the S100 family of calcium-binding proteins, is highly expressed in high-grade ductal carcinoma in situ (DCIS) and in the benign hyperproliferative skin disorder psoriasis. Both breast cancer and psoriasis are diseases which are characterized by hyperproliferation and a disturbed differentiation of the epithelial cells as well as a pronounced angiogenesis. The potential role of psoriasin in angiogenesis and the epithelial cell differentiation remain unclear.The aim of this thesis was to investigate the cellular effects of psoriasin in angiogenesis and the differentiation processes, with special emphasis on breast cancer and psoriasis.We found that psoriasin expression was induced in mammary epithelial cells and keratinocytes by oxidative stress. Psoriasin expression was shown to induce vascular endothelial growth factor (VEGF) expression and several other pro-angiogenic factors in epithelial cells. Upon down-regulation of psoriasin, H2O2-induced expression of VEGF was decreased as well as the pro-angiogenic factors heparin-binding EGF-like growth factor (HB-EGF) and matrix metalloproteinase (MMP)-1. Extracellular psoriasin contributed to the subsequent induction of proliferation, migration and tube formation of endothelial cells. The proliferative effect of psoriasin was shown to be mediated by the receptor for advanced glycation end products (RAGE). Furthermore, psoriasin induced reactive oxygen species (ROS) in both endothelial and epithelial cells through the action of RAGE, and contributed to the expression of the proangiogenic factors in endothelial cells.The expression of psoriasin was up-regulated in mammary epithelial cells and keratinocytes in response to differentiation-inducing stimuli and was shown to be regulated by pathways involved in epithelial cell differentiation. Upon psoriasin down-regulation the shift towards a more differentiated CD24+-phenotype of mammary epithelial cells was abolished. Furthermore, the expression of the differentiation markers involucrin, desmoglein 1, transglutaminase 1 and CD24 was decreased in keratinocytes upon down-regulation of psoriasin expression. ABSTRACT -II -In vivo we demonstrated a gradient of psoriasin expression in the psoriatic epidermis, with intense expression in the suprabasal differentiated layers, and a similar staining pattern between psoriasin and the differentiation marker CD24 in DCIS tumors.In conclusion, our findings describe psoriasin as a mediator in the angiogenic process and a contributor of epithelial cell differentiation. Consequently, psoriasin is possibly a contributor to the development and progression of breast cancer and psoriasis and a potential target in the treatment of these diseases. POPULÄRVETENSKAPLIG SAMMANFATTNING -III - POPULÄRVETENSKAPLIG SAMMANFATTNING BETYDELSEN AV PROTEINET PSORIASIN FÖR NYBILDNINGEN AV BLODKÄRL OCH UTMOGNADEN AV CELLER FÖR UTVECKLINGEN AV BRÖSTCANCER OCH PSORIASISBröstcancer är den vanligaste cancerformen bland kvinnor. I likhet med andra cancersjukd...

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S100A7 as a potential diagnostic and prognostic biomarker of esophageal squamous cell carcinoma promotes M2 macrophage infiltration and angiogenesis

Zheng

Liu

et al. 2021

Clinical & Translational Med

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Psoriasin (S100A7) increases the expression of ROS and VEGF and acts through RAGE to promote endothelial cell proliferation

Cited by 64 publications

References 43 publications

HMGB1, S100 proteins and other RAGE ligands in cancer - markers, mediators and putative therapeutic targets

HMGB1, S100 proteins and other RAGE ligands in cancer - markers, mediators and putative therapeutic targets

Psoriasin For Better or for Worse in Sickness and in Health : The Role of Psoriasin in Angiogenesis and Differentation of Epithelial Cells

S100A7 as a potential diagnostic and prognostic biomarker of esophageal squamous cell carcinoma promotes M2 macrophage infiltration and angiogenesis

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