Melanoma Research

1999

DOI: 10.1097/00008390-199904000-00001

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A synthetic peptide inhibitor for α-chemokines inhibits the tumour growth and pulmonary metastasis of human melanoma cells in nude mice

Nobumitsu Fujisawa

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,

Shinichiro Hayashi²,

Elmer S. Miller³

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Therapeutic Application Of Chemokines In Cancer1

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Cited by 24 publications

(16 citation statements)

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“…Previous studies have shown that antileukinate inhibited the binding of GROa and IL-8 to the receptors on neutrophils , melanoma cells (Hayashi et al 1997), melanocytes (Fujisawa et al 1999a) and endothelial cells (Fujisawa et al 1999b) in a dose-dependent manner.…”

Section: Discussionmentioning

confidence: 93%

“…The functions of these a-chemokines are mediated by speci®c receptors on the cell-surface membrane (Murphy and Tiany 1991;Moser et al 1993) and neutralizing antibodies against IL-8 or GROa inhibit IL-8-or GROa-induced angiogenesis or growth stimulation of melanoma cell lines (Arenberg et al 1996). Recently, we de®ned a novel hexapeptide, antileukinate (Ac-RRWWCR-NH 2 ), which is a potent inhibitor of a-chemokine binding to speci®c cell membrane receptors and can inhibit the growth of melanoma cells in vivo (Fujisawa et al 1999a). Therefore, we hypothesized that, by blocking a-chemokine binding to speci®c receptors on adenocarcinoma cells, antileukinate could act as a growth suppressant of adenocarcinoma tumors.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

α-Chemokine growth factors for adenocarcinomas; a synthetic peptide inhibitor for α-chemokines inhibits the growth of adenocarcinoma cell lines

³

et al. 2000

J Cancer Res Clin Oncol

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GROalpha and IL-8 are necessary for the growth of lung, stomach and colon adenocarcinomas, and can be inhibited by the hexapeptide, antileukinate. The findings suggest the possibility of using alpha-chemokine receptor inhibitors in the treatment of adenocarcinoma.

“…Previous studies have shown that antileukinate inhibited the binding of GROa and IL-8 to the receptors on neutrophils , melanoma cells (Hayashi et al 1997), melanocytes (Fujisawa et al 1999a) and endothelial cells (Fujisawa et al 1999b) in a dose-dependent manner.…”

Section: Discussionmentioning

confidence: 93%

“…The functions of these a-chemokines are mediated by speci®c receptors on the cell-surface membrane (Murphy and Tiany 1991;Moser et al 1993) and neutralizing antibodies against IL-8 or GROa inhibit IL-8-or GROa-induced angiogenesis or growth stimulation of melanoma cell lines (Arenberg et al 1996). Recently, we de®ned a novel hexapeptide, antileukinate (Ac-RRWWCR-NH 2 ), which is a potent inhibitor of a-chemokine binding to speci®c cell membrane receptors and can inhibit the growth of melanoma cells in vivo (Fujisawa et al 1999a). Therefore, we hypothesized that, by blocking a-chemokine binding to speci®c receptors on adenocarcinoma cells, antileukinate could act as a growth suppressant of adenocarcinoma tumors.…”

Section: Introductionmentioning

confidence: 99%

α-Chemokine growth factors for adenocarcinomas; a synthetic peptide inhibitor for α-chemokines inhibits the growth of adenocarcinoma cell lines

³

et al. 2000

J Cancer Res Clin Oncol

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GROalpha and IL-8 are necessary for the growth of lung, stomach and colon adenocarcinomas, and can be inhibited by the hexapeptide, antileukinate. The findings suggest the possibility of using alpha-chemokine receptor inhibitors in the treatment of adenocarcinoma.

“…and IL-8/CXCL8, called antileukinate (Fujisawa et al, 1999 and. Monoclonal antibodies against IL-8/CXCL8 and antileukinate inhibited tumor cell growth and pulmonary metastasis in vivo.…”

Section: Therapeutic Application Of Chemokines In Cancermentioning

confidence: 99%

The countercurrent principle in invasion and metastasis of cancer cells. Recent insights on the roles of chemokines

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,

2004

Int. J. Dev. Biol.

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Chemokine production by cancer cells constitutes a duality. Leukocyte recruitment under the pressure of chemokines may be beneficial for the host or for the tumor. Here, the emphasis will be on the detrimental effects of chemokines in tumor biology. A decade ago, the countercurrent principle of tumor-derived chemokine and peritumoral protease production was formulated to explain chemokine expression as a selective advantage for specific tumors and as a phenotype of invasive and metastasizing cancer cells. Chemoattracted leukocytes may provide trophic factors and produce invasion and metastasis-promoting proteinases. On the basis of the consensus sequence glutamic acid-leucine-arginine (ELR) preceding the canonical cysteine-any amino acidcysteine (CXC), ELR-positive CXC chemokines, such as interleukin-8 and granulocyte chemotactic protein-2, are angiogenic and thus instruct the host to feed the tumor and bring the vessels into closer contact with the tumor cells. These mechanisms may enhance lymphogenic and hematogenic metastasis. Recent research and proofs of this countercurrent concept are here reviewed and compared. In addition, we discuss how alterations in chemokine ligand and receptor expression profiles may contribute to tumor growth, invasion, metastasis and immune evasion. These comparisons imply practical consequences for future cancer diagnosis and therapy. The implications include methods to diminish metastasis by inhibiting angiogenic CXC chemokine ligands and receptors, therapeutic combinations of chemokine overexpression with antigenic stimuli and cotreatment with angiostatic chemokines and tumor antigens.

“…Mü ller et al (4) showed the involvement of CXCR4 and CCR7 in the metastatic behavior of breast cancer cells and the neutralizing potential of antibodies against CXCR4 was confirmed in a mouse model. Involvement of CXCR4 was also described in the migration and progression of human melanoma (5) and prostate cancer (6). Besides the correlation of CXCR4 expression on tumor cells with the formation of bone marrow metastasis, metastasis to lymph nodes has been shown to depend on the regulation of CCR6 and CCR7 expression in squamous cell carcinoma of the head and neck (7), on the expression of CCR7 in esophageal squamous carcinoma (8) and in non -small cell lung cancer (9), and on CXCR3 expression in a mouse model of melanoma (10).…”

mentioning

confidence: 96%

Up-Regulation of Functional Chemokine Receptor CCR3 in Human Renal Cell Carcinoma

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,

²

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³

et al. 2005

Clinical Cancer Research

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There is increasing evidence that chemokines and chemokine receptors are causally involved in tumorigenesis by facilitating tumor proliferation and metastasis. Little is known about the possible function of chemokine receptors in the development and progression of renal cell carcinoma (RCC). We, therefore, analyzed the expression of chemokine receptors in tumor specimens and adjacent healthy kidney tissues [normal kidney cell (NKC)] from 10 RCC patients.We also characterized the permanent RCC cell line A-498. CCR6, CXCR2, and CXCR3 were consistently expressed by both malignant cells and NKCs. A-498 displayed additional expression of CXCR4. Importantly, the expression of CCR3 was almost absent on NKCs but clearly enhanced in a substantial proportion of RCC specimens. The primary CCR3 ligand, eotaxin-1/CCL11, induced intracellular Ca 2+ mobilization, receptor internalization, and proliferation in A-498 cells confirming signaling competence of RCC-associated CCR3. In addition, we screened tumor tissue sections of 219 patients and found that 28% (62 of 219) expressed the CCR3 receptor. The presence of CCR3 in tumor samples seemed to correlate with the grade of malignancy. Previous work has established that eotaxin-1expression is induced by tumor necrosis factor-a, a cytokine known to be present in RCC tissue. Our data, therefore, supports a scenario in which eotaxin-1 as part of tumor-associated inflammation promotes progression and dissemination of CCR3-positive RCC.Cancers of the kidney account for 2% to 3% of all malignancies and have a peak incidence in the fifth and sixth decades of life. Renal cell carcinoma (RCC) is the most common malignant renal tumor with an incidence of 4 to 5 in 100 people. At diagnosis, 20% to 30% of the patients have metastatic disease and even a higher percentage of patients develop metachronous metastases after nephrectomy. When in metastatic progression, systemic therapies of RCC are largely ineffective in impacting disease response or patient survival. Therefore, defining the factors involved in disease progression and metastasis constitutes a necessary approach in the development of effective therapies.Multiple factors are known to contribute to the development and progression of neoplasias in general. Among them, chemokines are increasingly being recognized as key players (for reviews, see refs. 1, 2). Chemokines constitute a family of small (8-10 kDa) secreted proteins that act in paracrine or autocrine fashion. Most chemokines are expressed in response to stimuli [e.g., tumor necrosis factor-a (TNF-a) or IFN-g], but constitutive expression might also occur in a tissue-specific manner. Chemokines exert their activity via interaction with a large family of seven-transmembrane-spanning G protein -coupled receptors (3). There are f20 chemokine receptors described thus far and many of the receptors exhibit widespread binding properties. Thus, several chemokines can signal through the same receptor.Originally, chemokines were discovered as chemoattractants and activators of ...

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