Soluble CXCL16 promotes TNF‐α‐induced apoptosis in DLBCL via the AMAD10‐NF‐κB regulatory feedback loop

Yang, Hua; Qiu, Bo; Chen, Shaoying; Xiao, Yang; Chen, Minmin; Li, Wen‐Xing; Liao, Wanqin; El‐Ashram, Saeed; Yang, Anping; Liu, Fang

doi:10.1002/cbin.11154

Cited by 15 publications

(12 citation statements)

References 48 publications

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“…In a positive feedback loop, sCXC16 secretion promoted TNF- α production via the NF- κ B signalling pathway in DLBCL cells (Ref. 22). In addition to TNF- α , it has also been shown that IFN- γ stimulated CXCL16 production from tumour cells in prostate cancer (Ref.…”

Section: Cxcl16 Expression In Cancermentioning

confidence: 99%

CXC chemokine ligand 16: a Swiss army knife chemokine in cancer

Shabgah

Qasim

Mostafavi³

et al. 2021

Expert Rev. Mol. Med.

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Today, cancer is one of the leading causes of death worldwide. Lately, cytokine and chemokine imbalances have gained attention amongst different involved pathways in cancer development and attracted much consideration in cancer research. CXCL16, as a member of the CXC subgroup of chemokines, has been attributed to be responsible for immune cell infiltration into the tumour microenvironment. The aberrant expression of CXCL16 has been observed in various cancers. This chemokine has been shown to play a conflicting role in tumour development through inducing pro-inflammatory conditions. The infiltration of various immune and non-immune cells such as lymphocytes, cancer-associated fibroblasts and myeloid-derived suppressor cells by CXCL16 into the tumour microenvironment has complicated the tumour fate. Given this diverse role of CXCL16 in cancer, a better understanding of its function might build-up our knowledge about tumour biology. Hence, this study aimed to review the impact of CXCL16 in cancer and explored its therapeutic application. Consideration of these findings might provide opportunities to achieve novel approaches in cancer treatment and its prognosis.

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Section: Cxcl16 Expression In Cancermentioning

confidence: 99%

CXC chemokine ligand 16: a Swiss army knife chemokine in cancer

Shabgah

Qasim

Mostafavi³

et al. 2021

Expert Rev. Mol. Med.

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“…The complex environment of DLBCL possesses TNF-α along with chemokines and some cytokines produced in mesenchymal matrix from different inflammatory cells. In a recent study, it has been proved that sCXCL16 can reinforce TNF-α to mediate the DLBCL cell proliferation [34]. In this process, NF-κB signaling is activated by sCXCL16 to increase the production of TNF-α in DLBCL cells.…”

Section: Discussionmentioning

confidence: 99%

Cell type-specific Pathways Associated with Diffuse Large B-cell Lymphoma Metastasis Related to Neuro-Diseases

Dey¹,

Maulik²

2021

Preprint

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Background: With the advancement of single-cell sequencing, it’s become rapid emergency to detect the cell-specific changes of Diffuse Large B-cell Lymphoma metastasis that leads to the central nervous system disorder. Results: In this study, single-cell RNA-seq of Peripheral blood mononuclear cell from a human sample is curated and cell types related to lymphocytes are identified. Subsequently, the potential markers of Diffuse Large B-cell Lymphoma are found. It is noticed that LEF1, TCF7 and CD79A/B markers of different cell types show an important role in this disease formation, progression and metastasis processes. To understand the impact of markers, associated pathways are studied in details by establishing a pathway semantic network. Moreover, this association validated the channel through which the pathways are triggered within the cell environment and resulted in metastasis. The connection between Diffuse Large B-cell Lymphoma metastasis and other central nervous system disorders is demonstrated by constructing a disease network. Conclusion: The study reveals how cell types are responsible for the pathway shifts. Furthermore, this information provides a cell-specific channel of triggering the progression of central nervous system diseases among Diffuse Large B-cell Lymphoma patients.

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“…These results are in line with previous studies that demonstrated the capacity of CXCL16 to induce VEGF in human umbilical vein endothelial cells ( 38 , 39 ) and tumor cells ( 41 ). In addition, CXCL16 binding to its receptor CXCR6 induced upregulation of phospho-ERK1/2 in human umbilical vein endothelial cells ( 38 , 39 ) and activated the pro-inflammatory transcription factor NF-κB signaling pathway ( 68 ). These results suggest that one possible mechanism of CXCL16-induced pathological neovascularization in PDR is related to the upregulation of VEGF.…”

Section: Discussionmentioning

confidence: 99%

Evaluation of Proteoforms of the Transmembrane Chemokines CXCL16 and CX3CL1, Their Receptors, and Their Processing Metalloproteinases ADAM10 and ADAM17 in Proliferative Diabetic Retinopathy

et al. 2021

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The transmembrane chemokine pathways CXCL16/CXCR6 and CX3CL1/CX3CR1 are strongly implicated in inflammation and angiogenesis. We investigated the involvement of these chemokine pathways and their processing metalloproteinases ADAM10 and ADAM17 in the pathophysiology of proliferative diabetic retinopathy (PDR). Vitreous samples from 32 PDR and 24 non-diabetic patients, epiretinal membranes from 18 patients with PDR, rat retinas, human retinal Müller glial cells and human retinal microvascular endothelial cells (HRMECs) were studied by enzyme-linked immunosorbent assay, immunohistochemistry and Western blot analysis. In vitro angiogenesis assays were performed and the adherence of leukocytes to CXCL16-stimulated HRMECs was assessed. CXCL16, CX3CL1, ADAM10, ADAM17 and vascular endothelial growth factor (VEGF) levels were significantly increased in vitreous samples from PDR patients. The levels of CXCL16 were 417-fold higher than those of CX3CL1 in PDR vitreous samples. Significant positive correlations were found between the levels of VEGF and the levels of CXCL16, CX3CL1, ADAM10 and ADAM17. Significant positive correlations were detected between the numbers of blood vessels expressing CD31, reflecting the angiogenic activity of PDR epiretinal membranes, and the numbers of blood vessels and stromal cells expressing CXCL16, CXCR6, ADAM10 and ADAM17. CXCL16 induced upregulation of phospho-ERK1/2, p65 subunit of NF-κB and VEGF in cultured Müller cells and tumor necrosis factor-α induced upregulation of soluble CXCL16 and ADAM17 in Müller cells. Treatment of HRMECs with CXCL16 resulted in increased expression of intercellular adhesion molecule-1 (ICAM-1) and increased leukocyte adhesion to HRMECs. CXCL16 induced HRMEC proliferation, formation of sprouts from HRMEC spheroids and phosphorylation of ERK1/2. Intravitreal administration of CXCL16 in normal rats induced significant upregulation of the p65 subunit of NF-κB, VEGF and ICAM-1 in the retina. Our findings suggest that the chemokine axis CXCL16/CXCR6 and the processing metalloproteinases ADAM10 and ADAM17 might serve a role in the initiation and progression of PDR.

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Soluble CXCL16 promotes TNF‐α‐induced apoptosis in DLBCL via the AMAD10‐NF‐κB regulatory feedback loop

Cited by 15 publications

References 48 publications

CXC chemokine ligand 16: a Swiss army knife chemokine in cancer

CXC chemokine ligand 16: a Swiss army knife chemokine in cancer

Cell type-specific Pathways Associated with Diffuse Large B-cell Lymphoma Metastasis Related to Neuro-Diseases

Evaluation of Proteoforms of the Transmembrane Chemokines CXCL16 and CX3CL1, Their Receptors, and Their Processing Metalloproteinases ADAM10 and ADAM17 in Proliferative Diabetic Retinopathy

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