Chemokines and their role in tumor growth and metastasis

Wang, Ji Ming; Deng, Xiyun; Gong, Wanghua; Su, Shaobo

doi:10.1016/s0022-1759(98)00128-8

Cited by 279 publications

(203 citation statements)

References 86 publications

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“…Recent evidence suggests that these proteins can also regulate non-leukocyte cell functions such as angiogenesis/angiostasis, cell migration, activation of apoptotic cell death, and proliferation (Wang et al, 1998). Thus, we have investigated the expression of CXC-chemokine receptors on primary RCC cultures and on kidney cancer compared to normal kidney tissue, detecting an alteration of the CXCL12/CXCR4 signalling pathway in kidney cancer.…”

Section: Discussionmentioning

confidence: 99%

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CXCR4/CXCL12 expression and signalling in kidney cancer

et al. 2002

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CXCL12 (SDF-1), a CXC-chemokine, and its specific receptor, CXCR4, have recently been shown to be involved in tumourgenesis, proliferation and angiogenesis. Therefore, we analysed CXCL12α/CXCR4 expression and function in four human kidney cancer cell lines (A-498, CAKI-1, CAKI-2, HA-7), 10 freshly harvested human tumour samples and corresponding normal kidney tissue. While none of the analysed tumour cell lines expressed CXCL12α, A-498 cells were found to express CXCR4. More importantly, real-time RT–PCR analysis of 10 tumour samples and respective adjacent normal kidney tissue disclosed a distinct and divergent downregulation of CXCL12α and upregulation of CXCR4 in primary tumour tissue. To prove that the CXCR4 protein is functionally active, rhCXCL12α was investigated for its ability to induce changes of intracellular calcium levels in A-498 cells. Moreover, we used cDNA expression arrays to evaluate the biological influence of CXCL12α. Comparing gene expression profiles in rhCXCL12α stimulated vs unstimulated A-498 kidney cancer cells revealed specific regulation of 31 out of 1176 genes tested on a selected human cancer array, with a prominent stimulation of genes involved in cell-cycle regulation and apoptosis. The genetic changes reported here should provide new insights into the developmental paths leading to tumour progression and may also aid the design of new approaches to therapeutic intervention. British Journal of Cancer (2002) 86 , 1250–1256. DOI: 10.1038/sj/bjc/6600221 www.bjcancer.com © 2002 Cancer Research UK

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Section: Discussionmentioning

confidence: 99%

“…Chemokines constitute a superfamily of small pro-inflammatory cytokines that are involved in a variety of immune reactions including allergy, inflammation, infection, tissue injury, cardiovascular diseases and malignant tissue growth (Wang et al, 1998). Especially in solid tumours, recent research focused on the subfamily of a-or CXC-chemokines.…”

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confidence: 99%

CXCR4/CXCL12 expression and signalling in kidney cancer

et al. 2002

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“…Chemokines exert their effects by binding to 7 transmembrane domain G protein-coupled receptors. 11 receptors for the CC chemokines (CCR1-11) and 5 receptors for the CXC chemokines have been identified (Wang et al, 1998;Schweickart et al, 2000;Zlotnik and Yoshie, 2000). Their ligands bind to the extracellular N-terminus, leading to phosphorylation of serine/threonine residues on the cytoplasmic C-terminus, signalling and receptor desensitisation .…”

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confidence: 99%

Analysis of CC chemokine and chemokine receptor expression in solid ovarian tumours

Scotton¹,

Milliken

Wilson³

et al. 2001

Br J Cancer

100

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SummaryTo understand the chemokine network in a tissue, both chemokine and chemokine receptor expression should be studied. Human epithelial ovarian tumours express a range of chemokines but little is known about the expression and localisation of chemokine receptors. With the aim of understanding chemokine action in this cancer, we investigated receptors for CC-chemokines and their ligands in 25 biopsies of human ovarian cancer. CC-chemokine receptor mRNA was generally absent from solid tumours, the exception being CCR1 which was detected in samples from 75% of patients. CCR1 mRNA localised to macrophages and lymphocytes and there was a correlation between numbers of CD8 + and CCR1 expressing cells (P = 0.031). mRNA for 6 CC-chemokines was expressed in a majority of tumour samples. In a monocytic cell line in vitro, we found that CCR1 mRNA expression was increased 5-fold by hypoxia. We suggest that the CC-chemokine network in ovarian cancer is controlled at the level of CC-chemokine receptors and this may account for the phenotypes of infiltrating cells found in these tumours. The leukocyte infiltrate may contribute to tumour growth and spread by providing growth survival factors and matrix metalloproteases. Thus, CCR1 may be a novel therapeutic target in ovarian cancer.

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“…The main cause of death in patients with CRC is distant spread and organ metastasis [2]. The mechanisms behind cancer cell spread are not fully understood but convincing data indicate that increased expression of adhesion molecules and capacity to migrate in response to chemotactic stimuli are necessary for tumor cell metastasis [3]. Recent findings implicate that chemokines regulate multiple aspects of cancer cell biology, including proliferation, survival, angiogenesis, and migration [4].…”

Section: Introductionmentioning

confidence: 99%