Three-dimensional growth as multicellular spheroid activates the proangiogenic phenotype of colorectal carcinoma cells via LFA-1-dependent VEGF: implications on hepatic micrometastasis

Valcárcel, María; Arteta, Beatriz; Jaureguibeitia, Arrate; Lopategi, Aritz; Martínez, Iñigo; Mendoza, Lorea; Muruzábal, Francisco; Salado, Clarisa; Vidal‐Vanaclocha, Fernando

doi:10.1186/1479-5876-6-57

Cited by 67 publications

(55 citation statements)

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“…Expression of LFA-1 is a heterogeneous property of C26 cells that endows cancer cells with increased angiogenesis-stimulating potential. 19 Our current results indicate that LFA-1-expressing cancer cells also produce ManR-stimulating factors in response to ICAM-1. This may enable C26 cells to inhibit hepatic immune response through a ManRdependent mechanism.…”

Section: Discussionmentioning

confidence: 62%

“…Pretreatment of C26 cells with 2 lg/mL anti-murine LFA-1 antibodies for 45 minutes prior to coincubation with LSECs resulted in the same effect as ICAM-1 blockade. Anti-murine LFA-1 antibodies also decreased cancer cell attachment to LSECs, 19 suggesting that those C26 cells interacting with LSECs through other adhesion mechanisms were not involved in ManR and IL-1 up-regulation. As recently reported, 19 C26 cells expressed LFA-1 both in culture and during hepatic micrometastasis development in vivo.…”

Section: Resultsmentioning

confidence: 98%

“…Anti-murine LFA-1 antibodies also decreased cancer cell attachment to LSECs, 19 suggesting that those C26 cells interacting with LSECs through other adhesion mechanisms were not involved in ManR and IL-1 up-regulation. As recently reported, 19 C26 cells expressed LFA-1 both in culture and during hepatic micrometastasis development in vivo. Antibodies against other ICAM-1 ligands (Mac-1 and CD43) decreased neither tumor-dependent ManR-mediated endocytosis nor IL-1 production (Fig.…”

Section: Resultsmentioning

confidence: 98%

“…33 Moreover, ICAM-1-expressing hepatic myofibroblasts may further induce ManR-stimulating factor release from LFA-1-expressing colorectal cancer cells at metastatic sites. 19 Soluble ICAM-1 level is higher in patients with liver metastasis than in patients without liver metastasis. 34 Both tumor-and host-derived sICAM-1 promote immune escape 35 and angiogenic activity, 36 supporting tumor growth.…”

Section: Discussionmentioning

confidence: 99%

“…Hepatic metastases were produced and quantified as described. 19 In some experiments, C26 cells were pretreated in vitro with celecoxib as described above. ManR, ICAM-1, and alpha-smooth muscle actin (ASMA) expression were detected in frozen tissue sections using anti-CD206 monoclonal antibodies (Acris Antibodies, Hiddenhausen, Germany) detected with Alexa488-or Alexa595-conjugated secondary antibodies (Invitrogen, Carlsbad, CA), Cy3-conjugated anti-ASMA (Sigma Chemichal, St. Louis, MO), or Alexa488-conjugated ICAM-1 (Novus Biochemicals Inc., Littleton, CO).…”

Section: Methodsmentioning

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: Discussionmentioning

confidence: 62%

Section: Resultsmentioning

confidence: 98%

Section: Resultsmentioning

confidence: 98%

Section: Discussionmentioning

confidence: 99%

Section: Methodsmentioning

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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Basic Science of Liver Cancer Stem Cells and Hepatocarcinogenesis

Koch¹,

Leffert²

2015

Principles of Stem Cell Biology and Cancer

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Endothelial Differentiation and Vasculogenesis Induced by Three‐Dimensional Adipose‐Derived Stem Cells

Park

Kim

Jung

et al. 2012

The Anatomical Record

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Recently, an angiogenic therapy based on adipose-derived stem cells (ASCs) in an ischemic model has been reported. This study demonstrates the differentiation of human ASCs (hASCs) into endothelial cells clusters by culturing the cells in the form of three dimensional cell masses (3DCMs), which is based on the adherent activity of ASCs for a substrate. The 3DCM composed of hASCs induced hypoxic conditions and expressed angiogenic factors, such as vascular endothelial growth factor and interleukin-8. From immunochemical staining analysis, the 3DCMs of hASCs were CD31 þ , KDR þ , and CD34 þ , whereas monolayer-cultured hASCs were negative for the these markers. To evaluate the ability of vasculature to form within 3DCMs, the 3DCMs were mixed in Matrigel/fibrin gel and injected into mice. Mature tubular microvessels perfused with blood were observed in the 3DCM/gel 20 days after injection, but not in the gel alone or hASC/ gel mixture. Vasculature formed in the 3DCM/gel was recognized by antibodies against human a-smooth muscle actin, KDR, CD31, and CD34, but not by antibodies against murine antigens. These results suggest that the vasculatures originated from the embedded human cells. The 3DCMs of hASCs could function as a source of vascular cells for neovascularization, and could also be co-implanted with other cell types for regenerative medicine. Anat Rec,

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Three-dimensional growth as multicellular spheroid activates the proangiogenic phenotype of colorectal carcinoma cells via LFA-1-dependent VEGF: implications on hepatic micrometastasis

Cited by 67 publications

References 28 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

Basic Science of Liver Cancer Stem Cells and Hepatocarcinogenesis

Endothelial Differentiation and Vasculogenesis Induced by Three‐Dimensional Adipose‐Derived Stem Cells

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