Discrete roles of cytokines, TNF-α, IL-1, IL-6 in tumor promotion and cell transformation

Suganuma, Masami; Okabe, Sachiko; Kurusu, Miki; Iida, Naoyuki; Ohshima, Shiro; Saeki, Yukihiko; Kishimoto, Tadamitsu; Fujiki, Hirota

doi:10.3892/ijo.20.1.131

Cited by 49 publications

(48 citation statements)

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“…38,39 However, there are no significant differences in DMBA/TPA-induced papillomas between IL-6 ϩ/ϩ and IL-6 Ϫ/Ϫ C57/BL6 mice. 40 In the current study, TPA stimulated MCP-1 secretion by skin fibroblasts in vitro more effectively, rather than TNF-␣ and IL-6 ( Figure 4B), suggesting that the secretion of MCP-1 by fibroblast might play a role in skin tumor development. Therefore, the activation of an inflammatory tumor microenvironment may depend at least partly on fibroblasts.…”

Section: Discussionmentioning

confidence: 45%

FSP1+ Fibroblasts Promote Skin Carcinogenesis by Maintaining MCP-1-Mediated Macrophage Infiltration and Chronic Inflammation

Zhang

Chen

Xiao

et al. 2011

The American Journal of Pathology

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Cancer development is often associated with increased fibroblast proliferation and extensive fibrosis; however, the role of fibroblasts during carcinogenesis remains largely unknown. Using the 7,12-dimethylbenz-(a)anthracene and 12-O-tetradecanoylphorbol-13-acetateinduced two-stage skin carcinogenesis model, we demonstrated here that there was a massive accumulation and proliferation of fibroblasts in the skin shortly after application of carcinogen. Selective abatement of these cells during the promotion stage drastically decreased incidence and progression of papillomas. This correlated well with reduced macrophage infiltration and impaired cytokine storm in the affected skin. 12-O-tetradecanoylphorbol-13-acetate stimulated skin fibroblasts, secreting high levels of monocyte chemotactic protein-1, and neutralization of this chemokine eliminated almost completely the fibroblast-induced chemotaxis of macrophages. These results strongly suggest that fibroblasts promote skin tumor development by producing monocyte chemotactic protein-1 and maintaining chronic inflammation.

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Section: Discussionmentioning

confidence: 45%

FSP1+ Fibroblasts Promote Skin Carcinogenesis by Maintaining MCP-1-Mediated Macrophage Infiltration and Chronic Inflammation

Zhang

Chen

Xiao

et al. 2011

The American Journal of Pathology

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“…TNF-␣ can also be released by HM, for example, when these cells are stimulated with erythromycin (38) or by crocidolite as shown here. Although TNF-␣ was suspected to be a major player in MM pathogenesis (3,4,8,12) because it has been linked to carcinogenesis in other tumor models (22)(23)(24)(25) and to asbestos-induced fibrosis in animals (21), the possible mechanism by which TNF-␣ may contribute to MM had remained elusive.…”

Section: Discussionmentioning

confidence: 99%

“…In animal models of asbestosis, excess TNF-␣ has been shown to correlate with the development of fibrosis (20), and TNF-␣ receptor knockout mice do not develop fibroproliferative lesions after asbestos exposure (21). Moreover, there is convincing evidence in different experimental models that TNF-␣ is a critical mediator of tumor promotion and cell transformation (22)(23)(24)(25). Indeed, the existence of a link between chronic inflammation and certain types of cancer is now well established (26), and TNF-␣ has recently been found to be a crucial effecter of this link in various experimental models (27)(28)(29)(30).…”

mentioning

confidence: 99%

TNF-α inhibits asbestos-induced cytotoxicity via a NF-κB-dependent pathway, a possible mechanism for asbestos-induced oncogenesis

Yang

Bocchetta

Kroczyńska

et al. 2006

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

281

248

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“…Although TNF-α induces apoptosis, it also activates NF-κB, which inhibits apoptosis; therefore inhibitors of NF-κB may enhance the apoptotic activity of TNF-α . In addition, induction of proinflammatory cytokines via activation of NF-κB has been linked to tumor promotion (Suganuma et al, 2002), suggesting a further benefit of blocking NF-κB.…”

Section: Cancermentioning

confidence: 99%

Medicinal chemistry and pharmacology of genus Tripterygium (Celastraceae)

et al. 2007

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Plants in the genus Tripterygium, such as Tripterygium wilfordii Hook. f., have a long history of use in traditional Chinese medicine. In recent years there has been considerable interest in the use of Tripterygium extracts and of the main bioactive constituent, the diterpene triepoxide triptolide (1), to treat a variety of autoimmune and inflammation-related conditions. The main mode of action of the Tripterygium extracts and triptolide (1) is the inhibition of expression of proinflammatory genes such as those for interleukin-2 (IL-2), inducible nitric oxide synthase (iNOS), tumor necrosis factor-α (TNF-α), cyclooxygenase-2 (COX-2) and interferon-gamma (IFN-γ). The efficacy and safety of certain types of Tripterygium extracts were confirmed in human clinical trials in the US and abroad. Over 300 compounds have been identified in the genus Tripterygium, and many of these have been evaluated for biological activity. The overall activity of the extract is based on the interaction between its components. Therefore, the safety and efficacy of the extract cannot be fully mimicked by any individual constituent. This review discusses the biochemical composition and biological and pharmacological activities of Tripterygium extracts, and their main bioactive components.

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Discrete roles of cytokines, TNF-α, IL-1, IL-6 in tumor promotion and cell transformation

Cited by 49 publications

References 0 publications

FSP1+ Fibroblasts Promote Skin Carcinogenesis by Maintaining MCP-1-Mediated Macrophage Infiltration and Chronic Inflammation

FSP1+ Fibroblasts Promote Skin Carcinogenesis by Maintaining MCP-1-Mediated Macrophage Infiltration and Chronic Inflammation

TNF-α inhibits asbestos-induced cytotoxicity via a NF-κB-dependent pathway, a possible mechanism for asbestos-induced oncogenesis

Medicinal chemistry and pharmacology of genus Tripterygium (Celastraceae)

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