Chemokine Receptor CCR3 Expression in Malignant Cutaneous Tumors

Lee, Yoon Jin; Kim, Dae Hyun; Lee, Sang‐Han; Nam, Heerim; Roh, Mi Ryung; Cho, Moon Kyun

doi:10.5021/ad.2010.22.4.412

Cited by 6 publications

(6 citation statements)

References 21 publications

(25 reference statements)

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“…Expression of these four chemokine receptors is higher in human prostate cancer tissues when compared with normal epithelium or tissues presenting benign prostatic hyperplasia, and their expression could correlate with tumour aggressiveness 10 11 12 . More recently, it has been demonstrated that a prostate cancer cell line, Du-145, also expresses the CCR3 receptor 13 , whose over-expression was described previously in human melanoma or kidney cancers 14 15 . Chemokines are released by the tumour cells themselves and/or by host cells, including infiltrating leukocytes, endothelial cells and fibroblasts 8 9 .…”

mentioning

confidence: 62%

Periprostatic adipocytes act as a driving force for prostate cancer progression in obesity

Laurent

Guérard

Mazerolles³

et al. 2016

Nat Commun

207

185

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Obesity favours the occurrence of locally disseminated prostate cancer in the periprostatic adipose tissue (PPAT) surrounding the prostate gland. Here we show that adipocytes from PPAT support the directed migration of prostate cancer cells and that this event is strongly promoted by obesity. This process is dependent on the secretion of the chemokine CCL7 by adipocytes, which diffuses from PPAT to the peripheral zone of the prostate, stimulating the migration of CCR3 expressing tumour cells. In obesity, higher secretion of CCL7 by adipocytes facilitates extraprostatic extension. The observed increase in migration associated with obesity is totally abrogated when the CCR3/CCL7 axis is inhibited. In human prostate cancer tumours, expression of the CCR3 receptor is associated with the occurrence of aggressive disease with extended local dissemination and a higher risk of biochemical recurrence, highlighting the potential benefit of CCR3 antagonists in the treatment of prostate cancer.

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mentioning

confidence: 62%

Periprostatic adipocytes act as a driving force for prostate cancer progression in obesity

Laurent

Guérard

Mazerolles³

et al. 2016

Nat Commun

207

185

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“…CCR3 is increased in inflammatory cells that have infiltrated Hodgkin's lymphoma [20]. CCR3 is also associated with higher grades of malignancy in renal cell carcinoma [21], malignant cutaneous tumor [22], and glioblastoma [23]. More recently, it has been demonstrated that a prostate cancer cell line also expresses CCR3 and that the overexpression of CCR3 is significantly associated with cancer cell metastasis [14].…”

Section: Introductionmentioning

confidence: 99%

Crosstalk between CCL7 and CCR3 promotes metastasis of colon cancer cells via ERK-JNK signaling pathways

et al. 2016

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Chemokine ligand 7 (CCL7) enhances cancer progression and metastasis via epithelial-mesenchymal transition (EMT). However, little is known about the molecular mechanism of CCL7-induced EMT signaling cascade in colon cancer. Thus, the objective of this study was to investigate CCL7-induced EMT signaling pathway and its role in the progression and metastasis of colon cancer. To demonstrate the effect of CCL7 on EMT induction, HCT116 and HT29 cells overexpressing CCL7 were generated. CCL7-induced EMT and its downstream signaling pathway were evaluated by both in vitro and in vivo experiments. In in vitro studies, CCL7 was found to interplay with CC chemokine receptor 3 (CCR3), resulting in enhanced cellular proliferation, invasion, and migration via ERK and JNK signaling pathway. To validate these findings, we established ectopic and orthotopic mouse models injected with CCL7-overexpressed cells. In ectopic mouse models, we observed that CCL7-overexpressed cells grew significantly faster than control cells. In orthotopic mouse models, we found that liver and lung metastasis developed only in mice injected with CCL7-overexpressed cells. This study is the first one focusing on the EMT cascade via CCL7-CCR3-ERK-JNK signaling axis in colon cancer. Our novel findings will improve our understanding on the mechanism of metastatic process and provide potential therapeutic strategies for preventing metastasis in colon cancer.

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“…These receptors have been implicated in several diseases, including cancer [50][51][52]. For example, CCR1 expression in cancer cells is critical for fibroblasts to stimulate breast cancer cell proliferation [53], CCR2 exhibited a pro-tumor effect by stimulating the recruitment of monocytes/macrophages in lymphoma, melanoma, and breast cancer [54,55], and CCR3 was overexpressed in malignant cutaneous tumors, including malignant melanomas [56]. CCR3 expression in tumor tissues has been also shown to correlate with the grade of malignancy in human renal cancer [57].…”

Section: Discussionmentioning

confidence: 99%

CC Chemokine Ligand 7 Derived from Cancer-Stimulated Macrophages Promotes Ovarian Cancer Cell Invasion

Jeong

Wang

Choi

et al. 2021

Cancers

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In the tumor microenvironment, macrophages have been suggested to be stimulated by tumor cells, becoming tumor-associated macrophages that promote cancer development and progression. We examined the effect of these macrophages on human ovarian cancer cell invasion and found that conditioned medium of macrophages stimulated by ovarian cancer cells (OC-MQs) significantly increased cell invasion. CC chemokine ligand 7 (CCL7) expression and production were significantly higher in OC-MQs than in the control macrophages. Peritoneal macrophages from patients with ovarian cancer showed higher CCL7 expression levels than those from healthy controls. Inhibition of CCL7 using siRNA and neutralizing antibodies reduced the OC-MQ-CM-induced ovarian cancer cell invasion. CC chemokine receptor 3 (CCR3) was highly expressed in human ovarian cancer cells, and a specific inhibitor of this receptor reduced the OC-MQ-CM-induced invasion. Specific signaling and transcription factors were associated with enhanced CCL7 expression in OC-MQs. CCL7-induced invasion required the expression of matrix metalloproteinase 9 via activation of extracellular signal-related kinase signaling in human ovarian cancer cells. These data suggest that tumor-associated macrophages can affect human ovarian cancer metastasis via the CCL7/CCR3 axis.

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Chemokine Receptor CCR3 Expression in Malignant Cutaneous Tumors

Cited by 6 publications

References 21 publications

Periprostatic adipocytes act as a driving force for prostate cancer progression in obesity

Periprostatic adipocytes act as a driving force for prostate cancer progression in obesity

Crosstalk between CCL7 and CCR3 promotes metastasis of colon cancer cells via ERK-JNK signaling pathways

CC Chemokine Ligand 7 Derived from Cancer-Stimulated Macrophages Promotes Ovarian Cancer Cell Invasion

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