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Nakashima, Emi; Oya, Akiko; Kubota, Yoshi; Kanada, Naomi; Matsushita, Ryo; Takeda, Kazuyoshi; Ichimura, Fujio; Kuno, Kouji; Mukaida, Naofumi; Hirose, Kunitaka; Nakanishi, Isao; Ujiie, Toshimi; Matsushima, Kouji

doi:10.1023/a:1016057830271

Cited by 64 publications

(5 citation statements)

References 13 publications

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“… 43 CCL3 is a candidate for gene therapy, because its heterologous expression can enhance antitumor immune responses. 44 , 45 Recently, melanoma WNT/β-catenin signaling was shown to prevent antitumor immunity and CCL3 and CCL4 expression were repressed by high β-catenin expression. 46 Even though we did not see effects on CCL4 production by oncogenic CARMA1 in the absence of β-catenin, these data point out that β-catenin is able to repress the expression of chemokines that promote T-cell infiltration.…”

Section: Discussionmentioning

confidence: 99%

Oncogenic CARMA1 couples NF-κB and β-catenin signaling in diffuse large B-cell lymphomas

et al. 2016

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Constitutive activation of the antiapoptotic nuclear factor-κB (NF-κB) signaling pathway is a hallmark of the activated B-cell-like (ABC) subtype of diffuse large B-cell lymphomas (DLBCL). Recurrent oncogenic mutations are found in the scaffold protein CARMA1 (CARD11) that connects B-cell receptor (BCR) signaling to the canonical NF-κB pathway. We asked how far additional downstream processes are activated and contribute to the oncogenic potential of DLBCL-derived CARMA1 mutants. To this end, we expressed oncogenic CARMA1 in the NF-κB negative DLBCL lymphoma cell line BJAB. By a proteomic approach we identified recruitment of β-catenin and its destruction complex consisting of APC, AXIN1, CK1α and GSK3β to oncogenic CARMA1. Recruitment of the β-catenin destruction complex was independent of CARMA1-BCL10-MALT1 complex formation or constitutive NF-κB activation and promoted the stabilization of β-catenin. The β-catenin destruction complex was also recruited to CARMA1 in ABC DLBCL cell lines, which coincided with elevated β-catenin expression. In line, β-catenin was frequently detected in non-GCB DLBCL biopsies that rely on chronic BCR signaling. Increased β-catenin amounts alone were not sufficient to induce classical WNT target gene signatures, but could augment TCF/LEF-dependent transcriptional activation in response to WNT signaling. In conjunction with NF-κB, β-catenin enhanced expression of immunosuppressive interleukin-10 and suppressed antitumoral CCL3, indicating that β-catenin can induce a favorable tumor microenvironment. Thus, parallel activation of NF-κB and β-catenin signaling by gain-of-function mutations in CARMA1 augments WNT stimulation and is required for regulating the expression of distinct NF-κB target genes to trigger cell-intrinsic and extrinsic processes that promote DLBCL lymphomagenesis.

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Section: Discussionmentioning

confidence: 99%

Oncogenic CARMA1 couples NF-κB and β-catenin signaling in diffuse large B-cell lymphomas

et al. 2016

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“…When IL-8 is transfected in cancer cells, both tumor inhibition [152, 153] and promotion [126, 154] have been observed in vivo depending on the cell type [155]. …”

Section: Clinical Significancementioning

confidence: 99%

Recent Advances in Underlying Pathologies Provide Insight into Interleukin-8 Expression-Mediated Inflammation and Angiogenesis

Qazi

Tang

Qazi

2011

International Journal of Inflammation

195

125

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Interleukin-8 has long been recognized to have anti-inflammatory activity, which has been established in various models of infection, inflammation, and cancer. Several cell types express the receptor for the cytokine IL-8 and upon its recognition produce molecules that are active both locally and systemically. Many different types of cells, in particular monocytes, neutrophils, epithelial, fibroblast, endothelial, mesothelial, and tumor cells, secrete IL-8. Increased expression of IL-8 and/or its receptors has been characterized in many chronic inflammatory conditions, including psoriasis, ARDS, COPD, and RA as well as many cancers, and its upregulation often correlates with disease activity. IL-8 constitutes the CXC class of chemokines, a potent chemoattractant and activator of neutrophils and other immune cells. It is a proangiogenic cytokine that is overexpressed in many human cancers. Therefore, inhibiting the effects of IL-8 signaling may be a significant therapeutic intervention.

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“…When IL-8 is transfected in cancer cells, both tumor inhibition (Nakashima et al, 1996;Lee et al, 2000) and promotion (Luca et al, 1997;Inoue et al, 2000) have been observed in vivo, depending on the cell type.…”

Section: --------------------------------------------------------"mentioning

confidence: 99%

IL-8 expression and its possible relationship with estrogen-receptor-negative status of breast cancer cells

et al. 2003

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Estrogen-receptor (ER) status is an important parameter in breast cancer management as ER-positive breast cancers have a better prognosis than ER-negative tumors. This difference comes essentially from the lower aggressiveness and invasiveness of ER-positive tumors. Here, we demonstrate, that interleukin-8 (IL-8) was clearly overexpressed in most ER-negative breast, ovary cell lines and breast tumor samples tested, whereas no significant IL-8 level could be detected in ER-positive breast or ovarian cell lines. We have also cloned human IL-8 from ERnegative MDA-MB-231 cells, and we show that IL-8 produced by breast cancer cells is identical to monocytederived IL-8. Interestingly, the invasion potential of ERnegative breast cancer cells is associated at least in part with expression of IL-8, but not with IL-8 receptor levels. Moreover, IL-8 increases the invasiveness of ER-positive breast cancer cells by two fold, thus confirming the invasion-promoting role of IL-8. On the other hand, exogenous expression of estrogen receptors in ERnegative cells led to a decrease of IL-8 levels. In summary, our data show that IL-8 expression is negatively linked to ER status of breast and ovarian cancer cells. We also support the idea that IL-8 expression is associated with a higher invasiveness potential of cancer cells in vitro, which suggests that IL-8 could be a novel marker of tumor aggressiveness.

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Abstract: The rejection of the cells depends on cytolysis and generates potent and long lasting antitumor immunity. These data suggest that tumor cells transfected with the MIP-1 alpha gene might be useful as an effective therapy for the treatment of certain tumors.

Cited by 64 publications

References 13 publications

Oncogenic CARMA1 couples NF-κB and β-catenin signaling in diffuse large B-cell lymphomas

Oncogenic CARMA1 couples NF-κB and β-catenin signaling in diffuse large B-cell lymphomas

Recent Advances in Underlying Pathologies Provide Insight into Interleukin-8 Expression-Mediated Inflammation and Angiogenesis

IL-8 expression and its possible relationship with estrogen-receptor-negative status of breast cancer cells

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