Effects of micro-environment- and malignant cell-derived interleukin-1 in carcinogenesis, tumour invasiveness and tumour–host interactions

Apte, Ron N.; Krelin, Yakov; Song, Xiaoping; Dotan, Shahar; Recih, Eli; Elkabets, Moshe; Carmi, Yaron; Dvorkin, Tatyana; White, Roslayn M.; Gayvoronsky, Lubov; Segal, Shraga; Voronov, Elena

doi:10.1016/j.ejca.2006.01.010

Cited by 186 publications

(165 citation statements)

References 56 publications

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“…IL-1 levels are significantly increased in ductal invasive tissues as compared in benign tissues [11] and elevated levels of IL-1b are correlated with invasiveness and aggressiveness of breast cancer [37] and with a high tumour grade [13]. In addition to proliferation, IL-1 has been linked to invasion, angiogenesis and inhibition of apoptosis in cancer cells [14,15].…”

Section: Il-1 Family and Breast Cancermentioning

confidence: 99%

IL‐1 family in breast cancer: Potential interplay with leptin and other adipocytokines

2008

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Edited by Masayuki MiyasakaKeywords: IL-1 Leptin Adipocytokine Breast cancer Obesity a b s t r a c t Obesity is associated with an increased risk of breast cancer. interleukin-1 (IL-1), a pro-inflammatory cytokine secreted by adipose tissue, is involved in breast cancer development. There is also convincing evidence that other adipocytokines including leptin not only have a role in haematopoiesis, reproduction and immunity but are also growth factors in cancer. Therefore, IL-1 family and leptin family are adipocytokines which could represent a major link between obesity and breast cancer progression. This minireview provides insight into recent findings on the prognostic significance of IL-1 and leptin in mammary tumours, and discusses the potential interplay between IL-1 family members and adipocyte-derived hormones in breast cancer.

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Section: Il-1 Family and Breast Cancermentioning

confidence: 99%

IL‐1 family in breast cancer: Potential interplay with leptin and other adipocytokines

2008

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“…The link between unresolved inflammation and cancer has been well established with estimates that 15% of cancer deaths are inflammation-related [4]. Evidence for this link includes the following: a) some inflammatory diseases are associated with increased risk of cancer development; b) inflammatory mediators are present surrounding and within most tumors [5]; c) overexpression of inflammatory cytokines increases cancer development and progression in murine studies; d) inhibition of inflammatory mediators decreases cancer development and progression; and e) the use of nonsteroidal anti-inflammatory drugs (NSAIDs) has been found to decrease cancer incidence and delay progression in patients with breast, prostate, lung and colorectal cancers [6,7].…”

Section: Introductionmentioning

confidence: 99%

“…Experiments performed using fibrosarcoma cells transfected with the cDNA of activated IL-1β and transplanted into mice showed that tumor invasiveness positively correlated with the amount of IL-1β secreted [7]. In another study, mice were either treated with cells engineered to secrete IL-1β or exposed to lipopolysaccharide to induce IL-1β expression, prior to the injection of metastatic melanoma cells.…”

Section: Introductionmentioning

confidence: 99%

The Inflammatory Tumor Microenvironment, Epithelial Mesenchymal Transition and Lung Carcinogenesis

Heinrich

Walser

Krysan

et al. 2011

Cancer Microenvironment

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The inflammatory tumor microenvironment (TME) has many roles in tumor progression and metastasis, including creation of a hypoxic environment, increased angiogenesis and invasion, changes in expression of microRNAs (miRNAs) and an increase in a stem cell phenotype. Each of these has an impact on epithelial mesenchymal transition (EMT), particularly through the downregulation of E-cadherin. Here we review seminal work and recent findings linking the role of inflammation in the TME, EMT and lung cancer initiation, progression and metastasis.Finally, we discuss the potential of targeting aspects of inflammation and EMT in cancer prevention and treatment.

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“…However, the participation of tumor cells in the cytokine release, which is known to have important role in leukocyte/macrophage infiltration into the tumors and in organ-specific metastasis [39], cannot be excluded. For example, IL-1β affects the pattern of tumor-host interactions [40], and genetic ablation in mice results in absence of metastatic tumors in vivo [41]. Additionally, TNF-α up-regulates selectin overexpression on endothelial cells, which promotes tumor cell adhesion and migration [42,43].…”

Section: Discussionmentioning

confidence: 99%

Overexpression of NTPDase2 in gliomas promotes systemic inflammation and pulmonary injury

Braganhol

Zanin

Bernardi

et al. 2011

Purinergic Signalling

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Gliomas are the most common and devastating type of primary brain tumor. Many non-neoplastic cells, including immune cells, comprise the tumor microenvironment where they create a milieu that appears to dictate cancer development. ATP and the phosphohydrolytic products ADP and adenosine by activating P2 and P1 receptors may participate in these interactions among malignant and immune cells. Purinergic receptor-mediated cell communication is closely regulated by ectonucleotidases, such as by members of the ectonucleoside triphosphate diphosphohydrolase (E-NTPDase) family, which hydrolyze extracellular nucleotides. We have shown that gliomas, unlike astrocytes, exhibit low NTPDase activity.Furthermore, ATP induces glioma cell proliferation and the co-administration of apyrase decreases progression of injected cells in vivo. We have previously shown that NTPDase2 reconstitution dramatically increases tumor growth in vivo. Here we evaluated whether NTPDase2 reconstitution to gliomas modulates systemic inflammatory responses. We observed that NTPDase2 overexpression modulated pro-inflammatory cytokine production and platelet reactivity. Additionally, pathological alterations in the lungs were observed in rats bearing these tumors. Our results suggest that disruption of purinergic signaling via ADP accumulation creates an inflammatory state that may promote tumor spread and dictate clinical progression.

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Effects of micro-environment- and malignant cell-derived interleukin-1 in carcinogenesis, tumour invasiveness and tumour–host interactions

Cited by 186 publications

References 56 publications

IL‐1 family in breast cancer: Potential interplay with leptin and other adipocytokines

IL‐1 family in breast cancer: Potential interplay with leptin and other adipocytokines

The Inflammatory Tumor Microenvironment, Epithelial Mesenchymal Transition and Lung Carcinogenesis

Overexpression of NTPDase2 in gliomas promotes systemic inflammation and pulmonary injury

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