Tumor necrosis factor, cancer and anticancer therapy

Mocellin, Simone; Róssi, Carlo; Pilati, Pierluigi; Nitti, Donato

doi:10.1016/j.cytogfr.2004.11.001

Cited by 274 publications

(233 citation statements)

References 200 publications

(207 reference statements)

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“…Using real-time RT-PCR to analyze tumor cell expression of a cytokine panel, we found that whereas expression of chemotactic IL-1␤ and IL-6 was reduced in STAT1-induced cells, TNF-␣ was significantly increased. TNF-␣ is a well established promoter of chronic inflammatory disease and has also been demonstrated to promote tumor progression (58,59). A recent study demonstrated that STAT1 was capable of directly up-regulating TNF-␣, and this resulted in MDSC infiltration and inflammation-mediated cochlear destruction in a rat model of cisplatin-induced ototoxicity (53).…”

Section: Discussionmentioning

confidence: 99%

Tumor STAT1 Transcription Factor Activity Enhances Breast Tumor Growth and Immune Suppression Mediated by Myeloid-derived Suppressor Cells

Hix

Karavitis

Khan

et al. 2013

Journal of Biological Chemistry

113

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Background:The role of STAT1 in promoting tumor progression is not well understood. Results: STAT1 activity is elevated in human and mouse breast cancers, and STAT1 promotes breast cancer progression. Conclusion: Tumor STAT1 transcription factor activity enhances breast tumor growth and immune suppression mediated by MDSCs. Significance: STAT1 activity in breast cancer cells is responsible for shaping an immunosuppressive tumor microenvironment, and inhibiting STAT1 activity is a promising immune therapeutic approach.

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Section: Discussionmentioning

confidence: 99%

Tumor STAT1 Transcription Factor Activity Enhances Breast Tumor Growth and Immune Suppression Mediated by Myeloid-derived Suppressor Cells

Hix

Karavitis

Khan

et al. 2013

Journal of Biological Chemistry

113

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“…Cytokines and chemokines from tumor cells also modify their normal surrounding non-malignant stroma by modulating the function of epithelial cells, endothelial cells, fibroblasts and inflammatory cells to generate a supportive microenvironment [37][38][39]. For instance, TNFα, IL-6 and IL-17 were shown to promote tumor growth by modifying the function of stromal cells surrounding the tumor [40][41][42]. TNFα produced by tumor cells or inflammatory cells in the tumor microenvironment can promote tumor cell survival through the induction of NFκB-dependent anti-apoptotic molecules [43].…”

Section: Niche-dependent Neutrophil Functionmentioning

confidence: 99%

The Multifaceted Roles Neutrophils Play in the Tumor Microenvironment

Sionov

Fridlender

Granot

2014

Cancer Microenvironment

342

261

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Neutrophils are myeloid cells that constitute 50-70 % of all white blood cells in the human circulation. Traditionally, neutrophils are viewed as the first line of defense against infections and as a major component of the inflammatory process. In addition, accumulating evidence suggest that neutrophils may also play a key role in multiple aspects of cancer biology. The possible involvement of neutrophils in cancer prevention and promotion was already suggested more than half a century ago, however, despite being the major component of the immune system, their contribution has often been overshadowed by other immune components such as lymphocytes and macrophages. Neutrophils seem to have conflicting functions in cancer and can be classified into anti-tumor (N1) and pro-tumor (N2) sub-populations. The aim of this review is to discuss the varying nature of neutrophil function in the cancer microenvironment with a specific emphasis on the mechanisms that regulate neutrophil mobilization, recruitment and activation.

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“…[17][18][19][20][21][22][23] Several cytokines, including tumor necrosis factor (TNF), have been tested as anticancer agents either alone or in combination with common chemotherapeutics. 24 TNF is used in the clinic for isolated limb perfusion in patients suffering from advanced soft tissue sarcomas and melanomas 25,26 or for isolated perfusion of metastases. 27 Binding of TNF to its type I receptor (TNFR1) results in initiation of the extrinsic apoptotic pathway via caspase-8 cleavage.…”

mentioning

confidence: 99%

“…At the same time, TNF also elicits activation of NFjB, which induces prosurvival and inflammatory responses. 24 Antitumor properties of TNF relay on direct induction of apoptosis in cancer cells as well as on its antivascular effects; however, blood vessel necrosis and induction of a strong inflammatory response limits the clinical use of this cytokine. 24,27,28 Antitumor effects of TNF are enhanced by a combination of this cytokine with several classic chemotherapeutics.…”

mentioning

confidence: 99%

“…24 Antitumor properties of TNF relay on direct induction of apoptosis in cancer cells as well as on its antivascular effects; however, blood vessel necrosis and induction of a strong inflammatory response limits the clinical use of this cytokine. 24,27,28 Antitumor effects of TNF are enhanced by a combination of this cytokine with several classic chemotherapeutics. [29][30][31] Proteasome inhibition prevents NFjB activation, therefore, enhancing proapoptotic effects of TNF in many but not all cancer cell types.…”

mentioning

confidence: 99%

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TNF potentiates anticancer activity of bortezomib (Velcade®) through reduced expression of proteasome subunits and dysregulation of unfolded protein response

Nowis

McConnell

Dierlam

et al. 2007

Intl Journal of Cancer

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Bortezomib (Velcade 1 ) exploits proteasome inhibition as a unique mechanism of anticancer activity. The effectiveness of bortezomib is, however, limited, therefore, the search for therapeutic regimens combining bortezomib with other agents. In the present work we demonstrate enhanced anticancer activity of bortezomib by its combination with tumor necrosis factor (TNF) in the experimental model of C-26 colon carcinoma in mice. This interaction likely relies on the induction of a dysregulated response to ER stress, leading to apoptosis of cancer cells, evidenced by caspase-3 cleavage, p53 accumulation as well as increased SAPK/JNK phosphorylation. ER stress induced by the combination of TNF and bortezomib is corroborated by upregulation of BiP, PDI and calnexin as well as cleavage of caspase-12; however, in contrast to the classic pathway, it is also associated with decreased phosphorylation of eIF2a and prevention of XBP-1 splicing. TNF prevented the upregulation of Hsp27 induced by bortezomib, which may contribute to enhanced ER stress. Moreover, TNF interfered with bortezomib-induced upregulation of distinct subunits of the 26S proteasome. Bortezomib concentration used in this study was not sufficient to prevent TNF from inducing nuclear translocation of p65/RelA; however, the combination of both agents reduced total p65/RelA levels. Combined treatment of tumor-bearing mice with bortezomib and TNF not only inhibited tumor growth but also significantly prolonged animal survival. Therefore, combination of bortezomib with TNF is an attractive option for further clinical studies. ' 2007 Wiley-Liss, Inc.

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Tumor necrosis factor, cancer and anticancer therapy

Cited by 274 publications

References 200 publications

Tumor STAT1 Transcription Factor Activity Enhances Breast Tumor Growth and Immune Suppression Mediated by Myeloid-derived Suppressor Cells

Tumor STAT1 Transcription Factor Activity Enhances Breast Tumor Growth and Immune Suppression Mediated by Myeloid-derived Suppressor Cells

The Multifaceted Roles Neutrophils Play in the Tumor Microenvironment

TNF potentiates anticancer activity of bortezomib (Velcade®) through reduced expression of proteasome subunits and dysregulation of unfolded protein response

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