CXCL13 promotes intestinal tumorigenesis through the activation of epithelial AKT signaling

Zhao, Qun; Guo, Jian; Wang, Guizhen; Bi, Yunbo; Cheng, Xinran; Liao, Yixiang; Jin, S.; Li, Lian; Guo, Yang; Pan, Longrui; Zhang, Xudong; Tan, Yan; Lei, Yu

doi:10.1016/j.canlet.2021.04.012

Cited by 15 publications

(12 citation statements)

References 51 publications

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“…The CXCR5-mediated pathway also utilizes phosphoinositide 3-kinase (PI3K) to activate Akt, resulting in the activation of downstream NF-kB and mammalian target of rapamycin (mTOR) pathways involved in cell growth and invasion (52,53). Recent studies have found that CXCR5 regulates downstream glycogen synthase kinase-3b (GSK-3b) and b-catenin through the PI3K-Akt pathway, leading to epithelial cell proliferation and tumorigenesis through upregulating cyclin D1 and c-myc expressions (54). In addition to the ERK1/2 pathway, CXCR5 also activates the MAPK pathway utilizing c-Jun N-terminal kinase (JNK) and p38, to mediate prostate cancer cell proliferation and inflammatory pain, respectively (55,56).…”

Section: Cxcl13/cxcr5 Protein Structurementioning

confidence: 99%

Role of the CXCL13/CXCR5 Axis in Autoimmune Diseases

et al. 2022

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CXCL13 is a B-cell chemokine produced mainly by mesenchymal lymphoid tissue organizer cells, follicular dendritic cells, and human T follicular helper cells. By binding to its receptor, CXCR5, CXCL13 plays an important role in lymphoid neogenesis, lymphoid organization, and immune responses. Recent studies have found that CXCL13 and its receptor CXCR5 are implicated in the pathogenesis of several autoimmune diseases, such as rheumatoid arthritis, multiple sclerosis, systemic lupus erythematosus, primary Sjögren’s syndrome, myasthenia gravis, and inflammatory bowel disease. In this review, we discuss the biological features of CXCL13 and CXCR5 and the recent findings on the pathogenic roles of the CXCL13/CXCR5 axis in autoimmune diseases. Furthermore, we discuss the potential role of CXCL13 as a disease biomarker and therapeutic target in autoimmune diseases.

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Section: Cxcl13/cxcr5 Protein Structurementioning

confidence: 99%

Role of the CXCL13/CXCR5 Axis in Autoimmune Diseases

et al. 2022

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“…CXCL13 is also known as a B lymphocyte chemoattractant (BLC) or B cell-attracting chemokine 1 (BCA-1). It has been reported to be upregulated in human and mouse colon cancers [ 21 - 23 ] and in the serum of azoxymethane (AOM)/DSS-induced intestinal colorectal adenocarcinoma model compared to that in the control groups [ 24 ]. CXCL13 deficiency in mice showed a protective effect against intestinal injury by AOM/DSS treatment, whereas its activation was associated with inflammatory signaling pathways, such as AKT and nuclear factor kappa B (NF-κB) signaling [ 24 ].…”

Section: Resultsmentioning

confidence: 99%

The Probiotic Effects of the Saccharomyces cerevisiae 28-7 Strain Isolated from Nuruk in a DSS-Induced Colitis Mouse Model

Lee

2022

J. Microbiol. Biotechnol.

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Probiotics are microorganisms that can benefit host health when ingested in a live state, and lactic acid bacteria are the most common type. Among fungi, Saccharomyces boulardii (SB) is the only strain known to have a probiotic function with beneficial effects on colitis; however, information on other probiotic yeast strains is limited. Therefore, this study aimed to discover yeast strains expressing intestinal anti-inflammatory activities by exhibiting probiotic properties in dextran sodium sulfate (DSS)-induced colitis mice model. Nuruk (Korean traditional fermentation starter) containing various microbial strains was used as a source for yeast strains, and S. cerevisiae 28-7 (SC28-7) strain was selected with in vitro and in vivo characteristics to enable survival in the intestines. After 14 days of pretreatment with the yeast strains, DSS was co-administered for six days to induce colitis in mice. The results revealed that the disease activity index score was lowered by SC28-7 treatment compared to the DSS group, and the colon length and weight/length ratio were recovered in a pattern similar to that of the normal group. SC28-7 administration significantly reduced the secretion of pro-inflammatory cytokines in the serum and modified the mRNA expression of inflammatory cytokines (interleukin-1β, transforming growth factor-β, and interferon-γ) and proteins involved in gut barrier functions (mucin 2, mucin 3, zonula occludens-1, and occludin) in colon tissues. These results indicate that SC28-7 attenuates DSS-induced colon damage and inflammation, supporting its future use as a probiotic yeast for treating and preventing intestinal inflammatory diseases such as inflammatory bowel disease.

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“…CXCL13 is high in tumor tissue and is positively linked to a higher clinical stage. Accordingly, the median survival of patients with high CXCL13 expression is shorter than that of patients with low CXCL13 expression [175]. The underlying mechanism may be that TLR4-NF-κB signaling in DCs promotes CXCL13, invoked by intestinal microbiota translocation.…”

Section: Breast Cancermentioning

confidence: 99%

“…The underlying mechanism may be that TLR4-NF-κB signaling in DCs promotes CXCL13, invoked by intestinal microbiota translocation. And then the interaction of CXCL13 and CXCR5 regulates the AKT/GSK-3β/βcatenin pathway to upgrade Cyclin D1 and C-myc and support epithelial cell growth and intestinal tumorigenesis [175] (Table 2). In a separate study, Chen et al found that CXCL13-CXCR5 signaling was involved in tumor immunosuppression by histidine decarboxylase (HDC)-expressing bone marrow cells through regulation of Treg cells directly or indirectly affecting CD8 + T cells [135].…”

Section: Breast Cancermentioning

confidence: 99%