Expression of CX3CR1 associates with cellular migration, metastasis, and prognosis in human clear cell renal cell carcinoma

Yao, Xin; Qi, Lifeng; Chen, Xusheng; Du, Jie; Zhang, Zhenting; Liu, Suxiang

doi:10.1016/j.urolonc.2012.12.006

Cited by 48 publications

(52 citation statements)

References 21 publications

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“…These signatures may be related to the enhanced cellular motility or invasive ability and are reminiscent of the findings in a previous report by Chen et al describing the correlation between PD-L1 expression and epithelial—mesenchymal transition (EMT) [12]. We also found the substantial expression of several chemokines (CXCL1, CXCL5, CXCL8, and CX3CL1) related to cell migration, invasion, metastasis, or EMT [27–30], in KRAS -mutant lung adenocarcinoma cell lines, which was also dependent on MAPK signaling (unpublished data). Although the functional significance of these molecules requires further investigation, we speculate that MAPK signaling regulates gene expression related to EMT and immune evasion.…”

Section: Discussionsupporting

confidence: 85%

RAS–Mitogen-Activated Protein Kinase Signal Is Required for Enhanced PD-L1 Expression in Human Lung Cancers

et al. 2016

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Ectopic programmed cell death ligand 1 (PD-L1) expression in non-small cell lung cancers (NSCLCs) is related to immune evasion by cancer, and it is a molecular target of immune checkpoint therapies. Although some altered signals in NSCLCs are responsible for ectopic PD-L1 expression, the precise mechanisms remain obscure. Because we found a higher frequency of EGFR/KRAS mutations in NSCLC cell lines with high PD-L1 expression (p < 0.001), we evaluated the relationships between downstream signals and PD-L1 expression, particularly in three KRAS-mutant adenocarcinoma cell lines. The MEK inhibitor U0126 (20 μM) significantly decreased the surface PD-L1 levels by 50–60% compared with dimethyl sulfoxide (p < 0.0001). Phorbol 12-myristate 13-acetate stimulation (100 nM, 15 min) increased (p < 0.05) and two ERK2 siRNAs as well as KRAS siRNAs decreased (p < 0.05) PD-L1 expression. The transcriptional activity of the potential AP-1 site (+4785 to +5056 from the transcription start site) in the PD-L1 gene was demonstrated by luciferase assays, which was inhibited by U0126. The chromatin immunoprecipitation assay demonstrated the binding of cJUN to the AP-1 site. Two STAT3 siRNAs decreased PD-L1 expression by 10–32% in two of the three KRAS-mutant lung adenocarcinoma cell lines (p < 0.05), while the PI3K inhibitor LY294002 (40 μM) did not change the expression level. Supervised cluster analysis and gene set enrichment analysis between the PD-L1-high and -low NSCLCs revealed a correlation between PD-L1 expression and genes/pathways related to cell motility/adhesion. These results indicate that MAPK signaling is the dominant downstream signal responsible for ectopic PD-L1 expression, in which STAT3 is also involved to some extent. Furthermore, MAPK signaling may control the expression of PD-L1 and several genes related to enhanced cell motility. Our findings suggest that MAPK, along with STAT3, is important for determining PD-L1 expression, which could be useful for targeted therapies against lung cancers.

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Section: Discussionsupporting

confidence: 85%

RAS–Mitogen-Activated Protein Kinase Signal Is Required for Enhanced PD-L1 Expression in Human Lung Cancers

et al. 2016

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“…Among them, we identified matrix metalloproteinase 7, adhesion molecule CD44, vitronectin receptor (ITGAV), fractalkine receptor (CX3CR1), and transcription factor FoxC1, which are all known to promote the invasion and metastasis of solid tumors. 25,27,[35][36][37][38][39][40] Intriguingly, the increased expression of ITGAV, FoxC1, and CX3CR1 not only correlated with the elevated c-Jun level but also were enriched in secondary extranodal lymphoma. For personal use only.…”

Section: Discussionmentioning

confidence: 99%

Jun-regulated genes promote interaction of diffuse large B-cell lymphoma with the microenvironment

Blonska

Zhu

Chuang³

et al. 2015

Blood

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“…The human RCC 786-O cell line was maintained in RPMI 1640 medium supplemented with 10% FBS at 37˚C and 5% CO 2 . To determine the cellular growth curve, 5x10 4 cells suspended in 2 ml medium were seeded into a 6-well plate and cultured under normal conditions. At 24 or 48 h after seeding, the cells in each well were trypsinized and counted.…”

Section: Methodsmentioning

confidence: 99%

“…Treatment for this disease is difficult due to its high metastatic tendency, as well as its resistance to radiotherapy and chemotherapy (2). Patients with RCC develop metastasis in ~33% of cases (3), which causes ~35% of mortality (4)(5)(6). Recently, patients with RCC are being diagnosed at increasingly younger ages (7).…”

Section: Introductionmentioning

confidence: 99%

IL-8 induces the epithelial-mesenchymal transition of renal cell carcinoma cells through the activation of AKT signaling

Zhou

Liu

et al. 2016

Oncology Letters

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Abstract. The epithelial-mesenchymal transition (EMT) process has increasingly been examined due to its role in the progression of human tumors. Renal cell carcinoma (RCC) is one of the most common urological tumors that results in patient mortality. Previous studies have demonstrated that the EMT process is closely associated with the metastasis of RCC; however, the underlying molecular mechanism has not been determined yet. The present study revealed that interleukin (IL)-8 was highly expressed in metastatic RCC. IL-8 could induce the EMT of an RCC cell line by enhancing N-cadherin expression and decreasing E-cadherin expression. Furthermore, IL-8 could induce AKT phosphorylation, and the phosphatidylinositol-4,5-bisphosphate 3-kinase inhibitor LY294002 could inhibit the EMT of RCC cells that was induced by IL-8. Therefore, these results suggest that IL-8 is able to promote the EMT of RCC through the activation of the AKT signal transduction pathway, and this may provide a possible molecular mechanism for RCC metastasis.

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Expression of CX3CR1 associates with cellular migration, metastasis, and prognosis in human clear cell renal cell carcinoma

Cited by 48 publications

References 21 publications

RAS–Mitogen-Activated Protein Kinase Signal Is Required for Enhanced PD-L1 Expression in Human Lung Cancers

RAS–Mitogen-Activated Protein Kinase Signal Is Required for Enhanced PD-L1 Expression in Human Lung Cancers

Jun-regulated genes promote interaction of diffuse large B-cell lymphoma with the microenvironment

IL-8 induces the epithelial-mesenchymal transition of renal cell carcinoma cells through the activation of AKT signaling

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