Autocrine/paracrine mechanism of interleukin-17B receptor promotes breast tumorigenesis through NF-κB-mediated antiapoptotic pathway

Ck, Huang; Yang, Chunzhang; Jeng, Yung‐Ming; Cl, Chen; Hh, Wu; Chang, Yaoguang; C, Ma; Kuo, Wei-Ting; Kj, Chang; Jy, Shew; Wh, Lee

doi:10.1038/onc.2013.268

Cited by 90 publications

(96 citation statements)

References 36 publications

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“…IL-17RB epithelial expression in our study was not different between healthy control and CRC. An increased level of IL-17B, in light of an unchanged IL-17RB expression could result in an increase in the IL-17B-intitiated signaling in cancer tissue, which could potentially increase the tumourigenesis capacity as it was previously shown in breast cancer [25]. Consistent with an increased IL-17B in the stromal compartment, we found neutrophils as a source of IL-17B in CRC.…”

Section: Discussionsupporting

confidence: 75%

Distinctive expression pattern of interleukin-17 cytokine family members in colorectal cancer

et al. 2015

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Colorectal cancer (CRC) is one of the most common cancers in both genders. Even though interleukin (IL)-17A was shown to play an important role in intestinal tumourigenesis and CRC, other IL-17 family members were not studied well. We therefore studied the expression of IL-17 cytokine family members in CRC. Ten healthy colons and ten CRC mucosa were immunostained for IL-17B, IL-17C, IL-17E, and IL-17F, and their receptors IL-17RA, IL-17RB, and IL-17RC. Double immunofluorescence staining of the CRC mucosa was done for IL-17B with markers of neutrophils, endothelial cells, macrophages, T cells, mast cells, or fibroblasts. While IL-17B was increased in CRC with a strong presence both in the epithelial and stromal compartments, IL-17C showed different expression depending on the grade of differentiation and IL-17E remained unchanged. In contrast, IL-17F was decreased in CRC compared to healthy control. Colon epithelial cells stained positive for IL-17RA, IL-17RB, and IL-17RC in both healthy control and CRC. Neutrophils were the main source of IL-17B in the stroma. family members demonstrated distinct expression patterns in CRC, suggesting a differential role exerted by each member in colon carcinogenesis.

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Section: Discussionsupporting

confidence: 75%

Distinctive expression pattern of interleukin-17 cytokine family members in colorectal cancer

et al. 2015

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“…IL17RB signaling may provide an additional source of NF-kB activation whereas GPER1 and IGF1 activate AKT1 and MAPK signaling in marginal zone lymphoma and WM, respectively. 44,51,52 However, WNT5A is a suppressor of B-cell proliferation. 53 Many of the genes upregulated in the MYD88 L265P CXCR4…”

Section: Discussionmentioning

confidence: 99%

Transcriptome sequencing reveals a profile that corresponds to genomic variants in Waldenström macroglobulinemia

Hunter

Liu

Yang

et al. 2016

Blood

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• Transcription profiles associated with mutated MYD88, CXCR4, ARID1A, abnormal cytogenetics including 6q2, and familial WM are described.• Mutated CXCR4 profiles show impaired expression of the tumor suppressor response induced by MYD88 L265P and also G-protein/MAPK inhibitors.Whole-genome sequencing has identified highly prevalent somatic mutations including MYD88, CXCR4, and ARID1A in Waldenström macroglobulinemia (WM). The impact of these and other somatic mutations on transcriptional regulation in WM remains to be clarified. We performed next-generation transcriptional profiling in 57 WM patients and compared findings to healthy donor B cells. Compared with healthy donors, WM patient samples showed greatly enhanced expression of the VDJ recombination genes DNTT, RAG1, and RAG2, but not AICDA. Genes related to CXCR4 signaling were also upregulated and included CXCR4, CXCL12, and VCAM1 regardless of CXCR4 mutation status, indicating a potential role for CXCR4 signaling in all WM patients. The WM transcriptional profile was equally dissimilar to healthy memory B cells and circulating B cells likely due increased differentiation rather than cellular origin. The profile for CXCR4 mutations corresponded to diminished B-cell differentiation and suppression of tumor suppressors upregulated by MYD88 mutations in a manner associated with the suppression of TLR4 signaling relative to those mutated for MYD88 alone. Promoter methylation studies of top findings failed to explain this suppressive effect but identified aberrant methylation patterns in MYD88 wild-type patients. CXCR4 and MYD88 transcription were negatively correlated, demonstrated allele-specific transcription bias, and, along with CXCL13, were associated with bone marrow disease involvement. Distinct gene expression profiles for patients with wild-type MYD88, mutated ARID1A, familial predisposition to WM, chr6q deletions, chr3q amplifications, and trisomy 4 are also described. The findings provide novel insights into the molecular pathogenesis and opportunities for targeted therapeutic strategies for WM. (Blood. 2016;128(6):827-838)

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“…IL-17B has been shown to induce proinflammatory cytokine secretion by the THP-1 acute monocytic leukemic cell line, and to enhance inflammation, survival and metastasis in breast and pancreatic cancer [82, 83]. IL-17RB engagement in these cells recruited the Act1-TRAF6-TAK1 complex to the receptor [83].…”

Section: Il-17 Cytokine Signaling and Regulationmentioning

confidence: 99%

Interleukin 17 Family Cytokines: Signaling Mechanisms, Biological Activities, and Therapeutic Implications

Monin

Gaffen

2017

Cold Spring Harb Perspect Biol

264

235

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The cytokines of the IL-17 family play a central role in the control of infections, especially extracellular fungi. Conversely, if unrestrained, these inflammatory cytokines contribute to the pathology in numerous autoimmune and chronic inflammatory conditions. Recent advances have led to the approval of IL-17A-blocking biologics for the treatment of moderate to severe plaque psoriasis, but much remains to be understood about the biological functions, regulation and signaling pathways downstream of these factors. In this review, we outline the current knowledge on signal transduction and known physiological activities of IL-17 family cytokines. We will highlight in particular the current understanding of these cytokines in the context of skin manifestations of disease.

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Autocrine/paracrine mechanism of interleukin-17B receptor promotes breast tumorigenesis through NF-κB-mediated antiapoptotic pathway

Cited by 90 publications

References 36 publications

Distinctive expression pattern of interleukin-17 cytokine family members in colorectal cancer

Distinctive expression pattern of interleukin-17 cytokine family members in colorectal cancer

Transcriptome sequencing reveals a profile that corresponds to genomic variants in Waldenström macroglobulinemia

Interleukin 17 Family Cytokines: Signaling Mechanisms, Biological Activities, and Therapeutic Implications

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