Role of CX3CL1 in Diseases

Liu, Wangmi; Jiang, Libo; Bian, Chong; Liang, Yun; Rong, Xing; Yishakea, Mumingjiang; Dong, Jian

doi:10.1007/s00005-016-0395-9

Cited by 72 publications

(54 citation statements)

References 127 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…37 In gastric adenocarcinoma, tumor cells secreting CX3CL1 can recruit T cells and NK cells, thus, activating both the adaptive and innate immune responses, leading to prolonged survival. 38 Herein, we show that the IDH1-R132H mutation in gliomas is correlated with a better prognosis compared to wild-type gliomas. This difference was mainly mediated through CX3CL1/CX3CR1 chemotaxis, which recruits NK cells.…”

Section: Introductionmentioning

confidence: 96%

See 1 more Smart Citation

The R132H mutation in IDH1 promotes the recruitment of NK cells through CX3CL1/CX3CR1 chemotaxis and is correlated with a better prognosis in gliomas

et al. 2019

View full text Add to dashboard Cite

Mutations in the isocitrate dehydrogenase (IDH) 1 gene, especially the R132H mutation, have been reported to be associated with a better prognosis in glioma patients. However, the underlying molecular mechanisms are not yet well understood. Many factors may contribute to differences in the survival of IDH1 wild‐type and IDH1 mutant glioma patients, in which immune components play a potentially important role. In this study, we analyzed The Cancer Genome Atlas (TCGA), and the Chinese Glioma Genome Atlas (CGGA) databases, as well as glioma patient‐derived tumor samples. We found that there was a higher infiltration of natural killer (NK) cells in IDH1 mutant glioma patients, and this was correlated with a better prognosis. We also showed that IDH1‐R132 tumor cells had higher expression levels of the chemokine CX3CL1. This arises as a result of the conversion of α‐ketoglutarate to R(‐)‐2‐hydroxyglutarate by the IDH1 mutant and the resultant phosphorylation of nuclear factor kappa B. Knockdown of CX3CL1 decreased the migration of NK cells. In addition, the high levels of expression of CX3CL1 were positively correlated with glioma patient survival in the TCGA and CGGA databases, and in the clinical samples. Overall, our data have identified a novel mechanism in which R132H mutation of the IDH1 gene serves as a tumor suppressor by promoting the recruitment of NK cells through CX3CL1/CX3CR1 chemotaxis.

show abstract

Section: Introductionmentioning

confidence: 96%

“…demonstrated that CX3CL1/CX3CR1 can reduce the invasion of glioma cells . In gastric adenocarcinoma, tumor cells secreting CX3CL1 can recruit T cells and NK cells, thus, activating both the adaptive and innate immune responses, leading to prolonged survival …”

Section: Introductionmentioning

confidence: 99%

The R132H mutation in IDH1 promotes the recruitment of NK cells through CX3CL1/CX3CR1 chemotaxis and is correlated with a better prognosis in gliomas

et al. 2019

View full text Add to dashboard Cite

show abstract

“…Endothelium holds a crucial role regarding the expansion of inflammation, through expression of adhesion molecules such as selectins [55], the intracellular adhesion molecule-1 (ICAM-1) [56], and CX3CL1 (fractalkine) [57] that regulate inflammatory cell recruitment. The effect on vascular wall, along with the partly specified changes on glycocalyx [58], is increased permeability that in AKI, is expressed as proteinuria [58, 59].…”

Section: Introductionmentioning

confidence: 99%

Oxidative Stress and Acute Kidney Injury in Critical Illness: Pathophysiologic Mechanisms—Biomarkers—Interventions, and Future Perspectives

Pavlakou

Liakopoulos

Eleftheriadis

et al. 2017

Oxidative Medicine and Cellular Longevity

118

View full text Add to dashboard Cite

Acute kidney injury (AKI) is a multifactorial entity that occurs in a variety of clinical settings. Although AKI is not a usual reason for intensive care unit (ICU) admission, it often complicates critically ill patients' clinical course requiring renal replacement therapy progressing sometimes to end-stage renal disease and increasing mortality. The causes of AKI in the group of ICU patients are further complicated from damaged metabolic state, systemic inflammation, sepsis, and hemodynamic dysregulations, leading to an imbalance that generates oxidative stress response. Abundant experimental and to a less extent clinical data support the important role of oxidative stress-related mechanisms in the injury phase of AKI. The purpose of this article is to present the main pathophysiologic mechanisms of AKI in ICU patients focusing on the different aspects of oxidative stress generation, the available evidence of interventional measures for AKI prevention, biomarkers used in a clinical setting, and future perspectives in oxidative stress regulation.

show abstract

“…Recently, increasing evidence has indicated that CX3CL1 plays an important role in regulating cell invasion, proliferation and migration of inflammatory cells and various cancer cell lines (51). For example, the expression of CX3CL1 is associated with the metastatic rate and a poor prognosis of patients with prostate cancer (19).…”

Section: Discussionmentioning

confidence: 99%

ADAM17-regulated CX3CL1 expression produced by bone marrow endothelial cells promotes spinal metastasis from hepatocellular carcinoma

Sun

Wang

et al. 2020

Int J Oncol

Self Cite

View full text Add to dashboard Cite

Spinal metastasis occurs in 50-75% of bone metastases caused by hepatocellular carcinoma (HCC), and HCC-derived spinal metastasis can lead to a less favorable prognosis. Recently, several studies have demonstrated that C-X3-C motif chemokine ligand 1 (CX3CL1) is closely associated with cancer metastasis, and its secretion is modulated by a disintegrin and metalloproteinase 17 (ADAM17). Bone marrow endothelial cells (BMECs) are an essential component of bone marrow. However, little is known about the roles in and effects of BMECs on HCC spinal metastasis. The present study demonstrated that CX3CL1 and C-X-C motif chemokine receptor 3 (CXCR3) expression was upregulated in HCC spinal metastases, and that CX3CL1 promoted the migration and invasion of HCC cells to the spine. Western blot analysis revealed that the Src/protein tyrosine kinase 2 (PTK2) axis participated in CX3CL1-induced HCC cell invasion and migration. CX3CL1 also increased the expression of M2 macrophage markers in THP-1 monocytes. BMECs promoted the migration and invasion of Hep3B and MHCC97H cells by secreting soluble CX3CL1, whereas the neutralization of CX3CL1 inhibited this enhancement. CX3CL1 enhanced the activation of the phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha (PIK3CA)/AKT serine/threonine kinase 1 (AKT1) and Ras homolog family member A (RHOA)/Rho associated coiled-coil containing protein kinase 2 (ROCK2) signaling pathways through the Src/PTK2 signaling pathway. Furthermore, ADAM17 was activated by mitogen-activated protein kinase (MAPK) z14 in BMECs and significantly promoted the secretion of CX3CL1. HCC cells enhanced the recruitment and proliferation of BMECs. The overexpression of CX3CR1 facilitated the spinal metastasis of HCC in a mouse model in vivo. In addition, in vivo experiments revealed that BMECs promoted the growth of HCC in the spine. The present study demonstrated that CX3CL1 participates in HCC spinal metastasis, and that BMECs play an important role in the regulation of CX3CL1 in the spinal metastatic environment.

show abstract

Role of CX3CL1 in Diseases

Cited by 72 publications

References 127 publications

The R132H mutation in IDH1 promotes the recruitment of NK cells through CX3CL1/CX3CR1 chemotaxis and is correlated with a better prognosis in gliomas

The R132H mutation in IDH1 promotes the recruitment of NK cells through CX3CL1/CX3CR1 chemotaxis and is correlated with a better prognosis in gliomas

Oxidative Stress and Acute Kidney Injury in Critical Illness: Pathophysiologic Mechanisms—Biomarkers—Interventions, and Future Perspectives

ADAM17-regulated CX3CL1 expression produced by bone marrow endothelial cells promotes spinal metastasis from hepatocellular carcinoma

Contact Info

Product

Resources

About