Monocyte chemoattractant protein‐1 expression correlates with macrophage infiltration and tumor vascularity in human esophageal squamous cell carcinomas

Ohta, Makoto; Kitadai, Yasuhiko; Tanaka, Shinji; Yoshihara, Masaharu; Yasui, Wataru; Mukaida, Naofumi; Haruma, Ken; Chayama, Kazuaki

doi:10.1002/ijc.10705

Cited by 141 publications

(114 citation statements)

References 34 publications

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“…Furthermore, our data are in agreement with data reporting MCP-1 expression in a variety of human tumour cell lines including gastric, 10 ovarian, 45 breast, 9 melanoma, 46 pancreatic 7 and neuroblastoma cancer cell lines. 47 Similarly, in vivo, MCP-1 was expressed by tumour cells of different types including ovarian, 45,48 gastric, 10 pancreatic, 7 oesophageal 16,18 and also breast carcinoma cells. 8,9,17 More particularly in accordance with our results showing a selective expression of MCP-1 in invasive breast tumour cell lines, Valkovic et al 17 have shown that MCP-1 overexpression in tumour breast carcinoma 52,53 prostate cancer cells 54 and bladder cancer cells.…”

Section: Discussionmentioning

confidence: 96%

“…16 In tumours, MCP-1 is produced both by peritumoral stromal cells and by tumour cells themselves, but an overexpression of MCP-1 in invasive tumour cells has been documented in several human carcinomas including breast, gastric and oesophageal carcinomas. 10,17,18 If the functional implication of MCP-1 in tumour progression is therefore largely documented, the mechanisms regulating MCP-1 expression in tumour cells are still poorly understood.A major mechanism involved in the regulation of tumour-promoting genes by tumour cells is the loss of E-cadherin mediated cell-cell adhesion. 19,20 E-cadherin is a transmembrane glycoprotein found in adherens junctions implicated in the maintenance of a polarized and cohesive epithelium.…”

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confidence: 99%

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Transactivation of MCP‐1/CCL2 by β‐catenin/TCF‐4 in human breast cancer cells

Mestdagt

Polette

Butticè

et al. 2005

Intl Journal of Cancer

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The loss of E-cadherin expression and the translocation of b-catenin to the nucleus are frequently associated with the metastatic conversion of epithelial cells. In the nucleus, b-catenin binds to the TCF/LEF-1 (T-cell factor/ lymphoid enhancer factor) transcription factor family resulting in the activation of several genes, some of them having important implications in tumour progression. In our study, we investigated the potential regulation of monocyte chemotactic protein-1 (MCP-1/CCL2) expression by the b-catenin/TCF pathway. This CC-chemokine has been implicated in tumour progression events such as angiogenesis or tumour associated macrophage (TAM) infiltration. We thus demonstrated that MCP-1 expression correlates with the reorganization of the E-cadherin/b-catenin complexes. Indeed, MCP-1 was expressed by invasive breast cancer cells (MDA-MB-231, BT549 and Hs578T), which do not express E-cadherin but was not produced by noninvasive breast cancer cell lines (MCF7 and T47D) expressing high level of E-cadherin. In addition, the MCP-1 promoter was activated in BT549 breast cancer cells transfected with b-catenin and TCF-4 cDNAs. The MCP-1 mRNA level was similarly upregulated. Moreover, we showed that MCP-1 mRNA was downregulated after transfection with a siRNA against b-catenin in both BT549 and Hs578T cells. Our results therefore identify MCP-1 as a target of the b-catenin/TCF/LEF pathway in breast tumour cells, a regulation which could play a key role in breast tumour progression. ' 2005 Wiley-Liss, Inc.Key words: MCP-1; b-catenin; breast cancer Chemokines constitute a superfamily of proinflammatory cytokines that are implicated in tumour progression, modulating not only host tumour-specific immunological response but also angiogenesis or tumour cell invasion and proliferation. 1-3 Monocyte chemotactic protein-1 (MCP-1) or CCL2 is a CC-chemokine that specifically attracts monocytes and memory T cells. It has been particularly implicated in processes characterized by mononuclear cell infiltration including breast cancer. 4,5 In some models, MCP-1 has been shown to display an antitumoral effect. 6,7 Nevertheless, a large number of studies demonstrate that MCP-1 facilitates tumour progression through its ability to recruit stromal cells including tumour associated macrophages (TAMs) and endothelial cells. 7-10 A pro-angiogenic role of MCP-1 has been demonstrated in many systems, facilitating tumour growth and dissemination. 8,9,11,12 Moreover, a direct effect of MCP-1 on tumour cell migration in vitro has also been described. 13 Recently, Lebrecht et al. 14 have correlated an increased MCP-1 serum level with an advanced breast tumour stage and the presence of lymph node metastasis. In the same way, Amann et al. 15 reported a significant association between MCP-1 urinary levels and tumour stage and grade. They suggested a use of its urinary level as prognosis marker in bladder cancer. The correlation between MCP-1 expression and a poor prognosis was also demonstrated for the squamous cell carcinoma of the oeso...

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Section: Discussionmentioning

confidence: 96%

mentioning

confidence: 99%

Transactivation of MCP‐1/CCL2 by β‐catenin/TCF‐4 in human breast cancer cells

Mestdagt

Polette

Butticè

et al. 2005

Intl Journal of Cancer

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“…33 Multiple human tumors have also been showed to express high levels of MCP-1, [34][35][36] and MCP-1 could promote tumor progression and metastasis as well. [37][38][39] The immune cells, such as monocytes/macrophages and dendritic cells, are important constitutes for the microenvironment. 10 These cells rapidly recognize a wide variety of molecules expressed by pathogens, such as EBV.…”

Section: Lf Expression Levels Correlated Inversely With Mcp-1 and Il-mentioning

confidence: 99%

Lactoferrin suppresses the Epstein–Barr virus-induced inflammatory response by interfering with pattern recognition of TLR2 and TLR9

Zheng

Qin²,

Ye³

et al. 2014

Laboratory Investigation

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Epstein-Barr virus (EBV) infection contributes to tumorigenesis of various human malignancies including nasopharyngeal carcinoma (NPC). EBV triggers innate immune and inflammatory responses partly through Toll-like receptor (TLR) signaling. Lactoferrin (LF), with its anti-inflammatory properties, is an important component of the innate immune system. We previously reported that LF protects human B lymphocytes from EBV infection by its ability to bind to the EBV receptor CD21, but whether LF can suppress EBV-induced inflammation is unclear. Here, we report that LF reduced synthesis of IL-8 and monocyte chemoattractant protein-1 (MCP-1) induced by EBV in macrophages via its suppression of NF-kB activity. LF interacted with TLR2 and interfered with EBV-triggered TLR2-NF-kB activation. LF inhibited the ability of TLR9 to recognize dsDNA by binding to its co-receptor CD14, which blocked the interaction between CD14 and TLR9. EBV-induced inflammation was thus aggravated in the presence of CD14. In addition, LF expression levels were significantly downregulated in NPC specimens, and correlated inversely with IL-8 and MCP-1 expression. These findings suggest that LF may suppress the EBV-induced inflammatory response through interfering with the activation of TLR2 and TLR9.

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“…However, not only mast cells are capable of excreting MMPs and other pro-angiogenic factors, also tumor associated macrophages (TAMs), neutrophils and activated T lymphocytes can contribute to angiogenesis by releasing MMPs and angiogenic factors [127][128][129][130]. In a number of cancers, inflammatory cell infiltration correlated with the degree of tumor angiogenesis [131][132][133][134]. The role of inflammatory cell derived MMPs is largely the same compared to tumor cell derived MMPs.…”

Section: The Role Of Mmps In Tumor Angiogenesis and Tumor Growthmentioning

confidence: 99%