Interferons in the Treatment of Solid Tumors

Moschos, Stergios J.; Varanasi, Sai Manasa; Kirkwood, John M.

doi:10.1007/0-387-24361-5_9

Cited by 29 publications

(32 citation statements)

References 189 publications

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“…This may be of particular interest, as several Slfn genes appear to mediate growth inhibitory responses, and, therefore, deregulation of Slfn gene expression or other abnormalities in their function may contribute to the malignant phenotype. As our previous studies have demonstrated that Slfn genes are IFN-inducible (9, 18), we have examined the patterns of induction of different mouse Slfn genes and their functions, in malignant melanoma and renal cell carcinoma cells, diseases that exhibit relatively high sensitivity to IFN treatment as compared with several other malignancies (22)(23)(24).…”

Section: Discussionmentioning

confidence: 99%

Expression and Regulatory Effects of Murine Schlafen (Slfn) Genes in Malignant Melanoma and Renal Cell Carcinoma

Mavrommatis

Arslan

Sassano

et al. 2013

Journal of Biological Chemistry

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Background:The role of Slfn genes in antineoplastic responses is yet to be defined. Results: Murine Slfn genes are up-regulated in an IFN-dependent manner in melanoma, and RCC cells and members of this family differentially suppress proliferation and anchorage-independent malignant cell growth. Conclusion: Slfns play important roles in controlling malignant melanoma and RCC tumorigenesis. Significance: Modulation of Slfn expression may provide a novel approach for the treatment of malignancies.

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Section: Discussionmentioning

confidence: 99%

Expression and Regulatory Effects of Murine Schlafen (Slfn) Genes in Malignant Melanoma and Renal Cell Carcinoma

Mavrommatis

Arslan

Sassano

et al. 2013

Journal of Biological Chemistry

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“…These cytokines exhibit important regulatory effects on cell cycle progression, gene transcription, and mRNA translation (6 -11). Beyond their relevance in the regulation of innate responses, the important biological effects of IFNs have led to extensive clinical-translational work over the years that resulted in their introduction in clinical medicine as antiviral and antitumor agents, although they are also used in clinical neurology for the treatment of multiple sclerosis (4,12,13).…”

Section: Type I Interferons (Ifns)mentioning

confidence: 99%

Activation of Protein Kinase Cη by Type I Interferons

Redig

Sassano

Majchrzak-Kita

et al. 2009

Journal of Biological Chemistry

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“…IFNs are negative regulators of angiogenesis (Lindner, 2002;Caceres and Gonzalez, 2003). The efficacy of IFNs has been exploited in maintenance therapy for patients with various cell diseases, including cancers and leukemias (Guilhot et al, 2004;Borden, 2005;Moschos et al, 2005). The therapeutic potential of IFNs in association with other cytokines is currently under investigation (Lindner and Borden, 1997;Lindner, 2002;Caceres and Gonzalez, 2003).…”

Section: Introductionmentioning

confidence: 99%

Differential regulation of tumor necrosis factor-α-converting enzyme and angiotensin-converting enzyme by type I and II interferons in human normal and leukemic myeloid cells

et al. 2006

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The transmembrane metalloproteases angiotensin-converting enzyme (ACE) and tumor necrosis factor-a (TNF-a)-converting enzyme (TACE/ADAM-17) have been associated with inflammation, cancer progression and angiogenesis. Few investigations into the regulation of these enzymes by physiological stimuli have been reported. In this study, we investigated the influence of interferons (IFNs) type I (a, b) and II (c) on ACE and TACE expression of human leukemic NB4 cells and monocytes.We assessed the expression of proteases by reverse transcriptase-polymerase chain reaction, enzyme-linked immunosorbent assay and immunofluorescence analyses. IFNc, but not type I IFNs, upregulated membrane ACE in a dose-and time-dependency and this was reflected by the increase of ACE enzymatic activity and ACE mRNA. ACE upregulation was dependent on protein synthesis. Treatment of the interferon responsive factor 1 (IRF1)-unresponsive HepG2 cell line with IFNc did not affect ACE expression, thus suggesting the participation of the IRF1 signaling pathway in IFNc-mediated ACE upregulation in myeloid cells. In contrast, both types of IFNs, in a dose-and time-dependent manner, downregulated surface TACE without affecting TACE transcript. Soluble TACE was not detected in the medium of IFN-treated cells. IFNc-mediated decrease of surface TACE in NB4 cells was reversible, and correlated with an increase in intracellular TACE, suggesting that cell surface TACE was internalized in response to IFNs. These findings, showing the presence of IFN-dependent controlled mechanisms by which ACE and TACE levels are regulated in human normal and leukemic myeloid cells, may have implications in the context of current investigations on the therapeutic potential of IFNs.

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Interferons in the Treatment of Solid Tumors

Cited by 29 publications

References 189 publications

Expression and Regulatory Effects of Murine Schlafen (Slfn) Genes in Malignant Melanoma and Renal Cell Carcinoma

Expression and Regulatory Effects of Murine Schlafen (Slfn) Genes in Malignant Melanoma and Renal Cell Carcinoma

Activation of Protein Kinase Cη by Type I Interferons

Differential regulation of tumor necrosis factor-α-converting enzyme and angiotensin-converting enzyme by type I and II interferons in human normal and leukemic myeloid cells

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