Interleukin 1 (IL-1)-Dependent Melanoma Hepatic Metastasis In Vivo; Increased Endothelial Adherence by IL-1-Induced Mannose Receptors and Growth Factor Production In Vitro

Vidal‐Vanaclocha, Fernando; Álvarez, Antonia; Asumendi, Aintzane; Urcelay, B.; Tonino, Paola; Dinarello, Charles A.

doi:10.1093/jnci/88.3-4.198

Cited by 120 publications

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“…37 IL-1 has been implicated as a factor in tumor progression through induction of cancer cell adhesion and invasion, and through the stimulation of host cells to produce angiogenic and growth factors. 1,9,37 In our study, ManR up-regulation occurred in tumor-activated LSECs through an IL-1-dependent mechanism, and blockade of IL-1 effects by use of IL-1Ra abrogated ManR up-regulation induced by C26 colon cancer cells in vivo. IL-1Ra is a naturally occurring inhibitor to IL-1 that has been shown to decrease tumor growth and metastases, and the use of IL-1 inhibitors as a therapeutic approach in the treatment of cancer has been suggested.…”

Section: Discussionsupporting

confidence: 49%

“…6 Interestingly, this receptor uses a different binding domain to take up blood-borne collagen alpha chains, 7,8 and contributes to the adhesion of cancer cells to LSECs. [9][10][11] Furthermore, ManR is involved in antigen uptake, processing, and presentation to T cells by LSECs, 12 and it has been suggested that this process diminishes local immune response of the liver. 13 However, it is not known how ManR is regulated during the hepatic microvascular infiltration of cancer cells.…”

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confidence: 99%

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Colon carcinoma cell interaction with liver sinusoidal endothelium inhibits organ-specific antitumor immunity through interleukin-1-induced mannose receptor in mice

et al. 2010

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Mannose receptor (ManR)-mediated liver sinusoidal endothelial cell (LSEC) endocytosis plays a role in antigen presentation and innate immunity, but its role in hepatic metastasis is unknown. We studied ManR-mediated endocytosis during C26 colorectal cancer cell interaction with LSECs and its implications in metastasis. Uptake of labeled ManR ligands (mannan and ovalbumin) and immunohistochemistry were used to study ManR endocytosis and expression. Several interleukin (IL)-1 inhibitors and the cyclooxygenase-2 (COX-2) inhibitor celecoxib were used to analyze the role of IL-1 and COX-2 in ManR regulation. Anti-mouse ManR antibodies and ManR knockout (ManR 2/2 ) mice were used to identify ManR-dependent mechanisms during antitumor immune response of liver sinusoidal lymphocytes (LSLs) interacting with tumor-activated LSECs. ManR expression and endocytosis increased in tumor-activated LSECs through a two-step mechanism:(1) Release of COX-2-dependent IL-1-stimulating factors by lymphocyte function-associated antigen-1-expressing C26 cells in response to intercellular adhesion molecule-1 (ICAM-1), which was expressed and secreted by tumor-activated LSECs; and (2) widespread up-regulation of ManR in LSECs through tumor-induced IL-1. In addition, LSLs that had interacted with tumoractivated LSECs in vivo decreased their antitumor cytotoxicity and interferon (IFN)-gamma secretion while they increased IL-10 release ex vivo. IFN-gamma/IL-10 ratio also decreased in the hepatic blood from tumor-injected mice. Immunosuppressant effects of tumor-activated LSECs on LSLs were abrogated in both LSECs from ManR 2/2 mice and tumor-activated LSECs given antimouse ManR antibodies. Conclusion: ICAM-1-induced tumor COX-2 decreased antitumor activity during hepatic metastasis through IL-1-induced ManR. ManR constituted a common mediator for prometastatic effects of IL-1, COX-2, and ICAM-1. A rise in hepatic IFN-gamma/IL-10 ratio and antitumor cytotoxicity by way of ManR blockade is consistent with the antimetastatic effects of IL-1, COX-2, and ICAM-1 inhibitors. These data support ManR and ManR-stimulating factors as targets for hepatic colorectal metastasis therapy. (HEPATOLOGY 2010;51:2172-2182 Abbreviations: ASMA, alpha-smooth muscle actin; CM, cell-conditioned medium; COX-2, cyclooxygenase-2; CSPG, chondroitin sulfate proteoglycan; ELISA, enzyme-linked immunosorbent assay; FITC-OVA, fluorescein isothiocyanate-labeled ovalbumin; FSA, formaldehyde treated serum albumin; ICAM-1, intercellular adhesion molecule-1; ICE, IL-1-converting enzyme; IgG2a, immunoglobulin G2a; IL, interleukin; IL-1RI, IL-1 receptor type I; IL-1Ra, IL-1 receptor antagonist; LFA-1, lymphocyte function-associated antigen 1; LSEC, liver sinusoidal endothelial cell; LSL, liver sinusoidal lymphocyte; ManR, mannose receptor; ManR À/À , ManR knockout; SD, standard deviation; sICAM-1, soluble ICAM-1.From the

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Section: Discussionsupporting

confidence: 49%

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confidence: 99%

Colon carcinoma cell interaction with liver sinusoidal endothelium inhibits organ-specific antitumor immunity through interleukin-1-induced mannose receptor in mice

et al. 2010

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“…[D-6-3 H]-glucosamine hydrochloride (specific activity 0.37 used. 15 Cells were cultured in Dulbecco's modified Eagle's medium supplemented with 10% FCS, 100 U/mL penicillin, and 100 mg/mL streptomycin. Cultures were maintained at 37ЊC in a humidified Centrilobular 6 { 2* 6 { 4* atmosphere with 5% CO 2 .…”

Section: Methodsmentioning

confidence: 99%

“…They were identified as a desmin-expressing cell populausing a liquid scintillation b-counter. Cell number was also detertion (98% { 8%), in which half of the cells (50% { 6%) mined in parallel experiments using a previously described method, as follows 15 : cells were fixed in 80% (wt/vol) trichloroacetic acid expressed SMA, as quantified by flow cytometry (Fig. 4A).…”

Section: Methodsmentioning

confidence: 99%

Tumor-dependent activation of rodent hepatic stellate cells during experimental melanoma metastasis

et al. 1997

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in melanoma cell motility and invasion during hepatic metasIn this work we report the presence of intrametastatic tasis progression. (HEPATOLOGY 1997;26:634-642.) smooth-muscle iso-alpha-actin (SMA)-expressing cells which appeared from the early stages of the hepatic metastasis process of intrasplenically injected B16 melanoma (B16M) cells.The prominent desmoplastic fibroblast stroma seen in maThey formed a network of stromal cells among B16M cells, lignant neoplasms and in their derived metastases suggests a very low percentage of them expressing desmin. In contrast, that tumor-infiltrating fibroblasts play a role in cancer prothose parts of liver tissue unaffected by metastasis had perisi-gression 1 and metastasis. [2][3][4] Such fibroblasts are tumor-innusoidal desmin-expressing quiescent hepatic stellate cells duced and differ in a number of functional aspects from their (qHSC) which did not express SMA. Exposure of freshly iso-resting precursors; thus, in most cases they are myofilated rat quiesent hepatic stellate cells (qHSC) to B16M cell-broblast-like cells 5 expressing specific surface and cytoskeleconditioned medium (B16M-CM) leads to a progressive in-tal markers. 4 Moreover, their role may involve the secretion crease (P õ .01) in the number of SMA-expressing cells, which of specific proteins such as cytokines, 6 extracellular matrix was accompanied by a parallel reduction in the number of molecules 7,8 and proteases, 9,10 and the contraction of the tudesmin-expressing cells. In addition, B16M-CM also con-mor matrix, thereby facilitating tumor development 5 and retained chemotactic factor(s) which significantly (P õ .01) ducing the involvement of immune cell responses. 1 However, increased (50%) in vitro qHSC migration and stimulated both despite this plethora of information, further insights into the [ 3 H]thymidine and [ 3 H]glucosamine uptake in qHSC. More-specific origins and phenotypic heterogeneity, as well as into over, B16M-CM also significantly (P õ .01) enhanced qHSC the regulation and role of these cells, are lacking because of secretion of matrix metalloproteinase-2 (MMP-2), and un-the numerous types of existing tumors and sites of developknown chemotactic factor(s) enhancing in vitro migration of ment. B16M cells. The results suggest that B16 melanoma releasesThe liver is one of the first sites of primary or secondary qHSC-activating factors, which induce the appearance of me-oncogenesis, and numerous reports have also described the tastasis-infiltrating myofibroblasts by a paracrine mechanism. development of hepatic fibroblasts as myofibroblast-like cells Such cells showed cytoskeletal alterations which are associ-concomitantly with hepatocellular carcinoma. 11,12 Not surated with enhanced proliferation, glycosaminoglycan synthe-prisingly, the hepatic fibroblast population surrounding sinusis, MMP-2 secretion, and tumor-chemotactic factor produc-soids, i.e., the Ito, fat-storing, or hepatic stellate cells (HSC), tion. Thus, tumor-activated qHSC may play an important role constitutes a qu...

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“…A number of studies in murine tumor models have demonstrated the protumoral role of inflammatory mediators at distinct phases of malignant progression (5)(6)(7)(8). Conversely, inhibition of selected proinflammatory cytokines (e.g., TNF, IL1) or of inflammation-related transcription factors (e.g., NF-B) has resulted in reduced susceptibility to carcinogenesis and slower tumor development in experimental tumor models (7)(8)(9).…”

mentioning

confidence: 99%

Induction of a proinflammatory program in normal human thyrocytes by the RET/PTC1 oncogene

Borrello

Alberti

Fischer

et al. 2005

Proc. Natl. Acad. Sci. U.S.A.

306

260

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Rearrangements of the RET receptor tyrosine kinase gene generating RET͞PTC oncogenes are specific to papillary thyroid carcinoma (PTC), the most frequent thyroid tumor. Here, we show that the RET͞PTC1 oncogene, when exogenously expressed in primary normal human thyrocytes, induces the expression of a large set of genes involved in inflammation and tumor invasion, including those encoding chemokines (CCL2, CCL20, CXCL8, and CXCL12), chemokine receptors (CXCR4), cytokines (IL1B, CSF-1, GM-CSF, and G-CSF), matrix-degrading enzymes (metalloproteases and urokinase-type plasminogen activator and its receptor), and adhesion molecules (L-selectin). This effect is strictly dependent on the presence of the RET͞PTC1 Tyr-451 (corresponding to RET Tyr-1062 multidocking site). Selected relevant genes (CCL20, CCL2, CXCL8, CXCR4, L-selectin, GM-CSF, IL1B, MMP9, UPA, and SPP1͞OPN) were found up-regulated also in clinical samples of PTC, particularly those characterized by RET͞PTC activation, local extrathyroid spread, and lymph node metastases, when compared with normal thyroid tissue or follicular thyroid carcinoma. These results, demonstrating that the RET͞PTC1 oncogene activates a proinflammatory program, provide a direct link between a transforming human oncogene, inflammation, and malignant behavior.chemokines ͉ inflammation ͉ papillary thyroid carcinoma ͉ gene expression

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Interleukin 1 (IL-1)-Dependent Melanoma Hepatic Metastasis In Vivo; Increased Endothelial Adherence by IL-1-Induced Mannose Receptors and Growth Factor Production In Vitro

Abstract: Given the multiple and complex cytokine cascade induced in vivo and in vitro during LPS-induced systemic inflammation, IL-1 plays a strategic role. Since IL-1Ra is without side effects in humans, studies on intraoperative infusion of IL-1Ra during tumor resection may be indicated.

Cited by 120 publications

References 0 publications

Colon carcinoma cell interaction with liver sinusoidal endothelium inhibits organ-specific antitumor immunity through interleukin-1-induced mannose receptor in mice

Colon carcinoma cell interaction with liver sinusoidal endothelium inhibits organ-specific antitumor immunity through interleukin-1-induced mannose receptor in mice

Tumor-dependent activation of rodent hepatic stellate cells during experimental melanoma metastasis

Induction of a proinflammatory program in normal human thyrocytes by the RET/PTC1 oncogene

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