Infiltration of COX-2–expressing macrophages is a prerequisite for IL-1β–induced neovascularization and tumor growth

Nakao, Shintaro; Kuwano, Takashi; Tsutsumi-Miyahara, Chikako; Ueda, Shu Ichi; Kimura, Yusuke; Hamano, Shinjiro; Sonoda, Koh Hei; Saijo, Yasuo; Nukiwa, Toshihiro; Strieter, Robert M.; Ishibashi, Tatsuro; Kuwano, Michihiko; Ono, Masahiro

doi:10.1172/jci23298

Cited by 264 publications

(243 citation statements)

References 51 publications

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“…76,77 For example, COX2-expressing macrophages infiltrate the LLC tumors expressing the inflammatory cytokine IL-1a, and they are required for angiogenesis and tumor progression mediated by this cytokine. 78 These findings highlight the crucial role of macrophages in inflammationmediated tumor vascularization and progression.…”

Section: Inflammation and Metastasismentioning

confidence: 93%

Inflammation and skeletal metastasis

Roca

McCauley

2015

BoneKEy Reports

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On the road to metastasis a cancer cell has to overcome two major obstacles: the physical escape from the primary tumor to a distant tissue and the adaptation to the new microenvironment via colonization and the formation of a secondary tumor. Accumulated scientific findings support the hypothesis that inflammation is a critical component of the tumor microenvironment and develops as a result of tumor-induced recruitment of inflammatory cells and their reciprocal interaction with other cells from the tumor network. These interactions modulate immune responses to suppress antitumor immunity and activate feedback amplification signaling loops that link nearly all the cells in the cancer inflammatory milieu. The coordinated regulation of cytokines/chemokines, receptors and other inflammatory mediators enables the different steps of the metastatic cascade. As a target organ for colonization, the bone is rich in inflammatory mediators that are critical for successful cancer growth. In this review, we focus on the inflammatory cells, molecules and mechanisms that facilitate the expansion of cancer cells from the primary tumor to their new 'home' in the skeleton.

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Section: Inflammation and Metastasismentioning

confidence: 93%

Inflammation and skeletal metastasis

Roca

McCauley

2015

BoneKEy Reports

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“…22,23 Importantly, IL-1b was shown to control tumor angiogenesis and invasiveness of different tumor cells in mice. 24,25 Moreover, IL-1b plays a role in destructive joint and bone diseases. In particular, IL-1b induces production of collagenase by synovial cells and of metalloproteinases by chondrocytes.…”

Section: Caspase-1 and It Substrate Il-1bmentioning

confidence: 99%

Inflammatory caspases and inflammasomes: master switches of inflammation

2006

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Fifteen years have passed since the cloning and characterization of the interleukin-1b-converting enzyme (ICE/caspase-1), the first identified member of a family of proteases currently known as caspases. Caspase-1 is the prototypical member of a subclass of caspases involved in cytokine maturation termed inflammatory caspases that also include caspase-4 caspase -5, caspase -11 and caspase -12. Efforts to elucidate the molecular mechanisms involved in the activation of these proteases have uncovered an important role for the NLR family members, NALPs, NAIP and IPAF. These proteins promote the assembly of multiprotein complexes termed inflammasomes, which are required for activation of inflammatory caspases. This article will review some evolutionary aspects, biochemical evidences and genetic studies, underlining the role of inflammasomes and inflammatory caspases in innate immunity against pathogens, autoinflammatory syndromes and in the biology of reproduction. Inflammatory CaspasesThe history of caspases began with the identification of an aspartate-specific protease activity involved in the conversion of the 31 kDa proIL-1b precursor to its active 17 kDa biologically active form, 1,2 and the identification of caspase-1 as the protease responsible for proIL-1b maturation. 3,4 The subsequent discovery of ced-3, that shares similarities with caspase-1 and which is involved in programmed cell death (PCD) in Caenorhabditis elegans, suggested that caspases might play fundamental roles in apoptosis. 5 As reviewed in the papers accompanying this issue of Cell Death and Differentiation, the role of apoptotic caspases in C. elegans and in vertebrates is crucial and deal with many facets of cell biology, development and diseases. In this review, we will focus on a subset of caspases present only in vertebrates and known as inflammatory caspases.Inflammatory caspases (also known as group I caspases) are encoded by three main genes in humans caspase-1, caspase-4 and caspase-5 and three main genes in mouse, caspase-1, caspase-11 and caspase-12. 6,7 In mammals, these caspases are characterized by the presence of a CARD domain at the N-terminus (Figure 1a). Human, chimp and mouse inflammatory caspases share significant similarity and are organized in a single locus (Figure 1c). Phylogenetic analysis of the conserved CARD domain suggests that the inflammatory caspases can be separated in evolutionaryrelated clusters (Figure 1b). The caspase-1 cluster contains caspase-1 and four other genes encoding decoy caspases: cop, inca1, inca2 and iceberg. These decoy caspase-1-like genes are absent in the mouse genome, suggesting that they have arisen recently by duplication of caspase-1. Although human and mouse caspase-1 are likely orthologues, sequence analysis suggests that human caspase-4 and caspase-5 have originated from a duplication of caspase-11. 7 However, the human caspase-12 gene, which in the chimp genome contains an SHG box important for it enzymatic activity, 8 evolved towards an enzymatically inactive form at some stage...

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“…It would be interesting to know whether IL-1 can induce COX2 in normal and cancerous prostate cells. Furthermore, IL-1 was shown to induce matrix metalloproteinases and pro-angiogenic factors in different cells, including cancer cells, and thus it may contribute to altering tissue microenvironment and homeostasis [28,29]. These features of IL-1 might also positively cooperate with tumor development, progression and metastasis in the prostate gland.…”

Section: Il-1 and Il-18mentioning

confidence: 99%

Role of inflammasomes and their regulators in prostate cancer initiation, progression and metastasis

Veeranki

2013

Cellular and Molecular Biology Letters

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Prostate cancer is one of the main cancers that affect men, especially older men. Though there has been considerable progress in understanding the progression of prostate cancer, the drivers of its development need to be studied more comprehensively. The emergence of resistant forms has also increased the clinical challenges involved in the treatment of prostate cancer. Recent evidence has suggested that inflammation might play an important role at various stages of cancer development. This review focuses on inflammasome research that is relevant to prostate cancer and indicates future avenues of study into its effective prevention and treatment through inflammasome regulation. With regard to prostate cancer, such research is still in its early stages. Further study is certainly necessary to gain a broader understanding of prostate cancer development and to create successful therapy solutions.

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Infiltration of COX-2–expressing macrophages is a prerequisite for IL-1β–induced neovascularization and tumor growth

Cited by 264 publications

References 51 publications

Inflammation and skeletal metastasis

Inflammation and skeletal metastasis

Inflammatory caspases and inflammasomes: master switches of inflammation

Role of inflammasomes and their regulators in prostate cancer initiation, progression and metastasis

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