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Chawla‐Sarkar, Mamta; Lindner, Daniel J.; Yf, Liu; Williams, Bryan R.G.; Sen, Ganes C.; Silverman, Robert H.; Borden, Ernest C.

doi:10.1023/a:1023668705040

Cited by 732 publications

(249 citation statements)

References 91 publications

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“…Therefore, increased knowledge of the physiological mechanisms by which ACE and TACE are regulated is of particular interest in view of the comprehension of their roles in diseased conditions. Interferons (IFNs) belong to a family of cytokines that are implicated in anti-viral, anti-proliferative, antitumoral and immunomodulatory effects (Stark et al, 1998;Chawla-Sarkar et al, 2003). IFNs are negative regulators of angiogenesis (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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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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“…Interferons (IFNs) are a family of cytokines that have multiple biological effects including immunomodulatory, antiviral, antiproliferative, antigen modulation, cell differentiation, and apoptotic effects (Pestka et al, 1987;Stark et al, 1998;Chawla-Sarkar et al, 2003). Upon secretion from cells, IFNs bind to specific cell membrane receptors and activate the JAK-STAT pathway, which results in upregulation of IFN-stimulated genes (ISGs) (Darnell et al, 1994;Stark et al, 1998).…”

Section: Introductionmentioning

confidence: 99%

Interferon-regulatory factor-1 is critical for tamoxifen-mediated apoptosis in human mammary epithelial cells

et al. 2004

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Unlike estrogen receptor-positive (ER( þ )) breast cancers, normal human mammary epithelial cells (HMECs) typically express low nuclear levels of ER (ER poor). We previously demonstrated that 1.0 lM tamoxifen (Tam) promotes apoptosis in acutely damaged ER-poor HMECs through a rapid, 'nonclassic' signaling pathway. Interferon-regulatory factor-1 (IRF-1), a target of signal transducer and activator of transcription-1 transcriptional regulation, has been shown to promote apoptosis following DNA damage. Here we show that 1.0 lM Tam promotes apoptosis in acutely damaged ER-poor HMECs through IRF-1 induction and caspase-1/3 activation. Treatment of acutely damaged HMEC-E6 cells with 1.0 lM Tam resulted in recruitment of CBP to the c-IFN-activated sequence element of the IRF-1 promoter, induction of IRF-1, and sequential activation of caspase-1 and -3. The effects of Tam were blocked by expression of siRNA directed against IRF-1 and caspase-1 inhibitors. These data indicate that Tam induces apoptosis in HMEC-E6 cells through a novel IRF-1-mediated signaling pathway that results in activated caspase-1 and -3.

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“…IFNs are also negative regulators of angiogenesis (Singh et al, 1995) and a possible role of apoptosis in mediating the antitumor effects of IFNs has been postulated (Chawla-Sarkar et al, 2003). IFNs alone or combined with other antitumor drugs are now used in cancer therapies and new applications are under investigation (Wadler and Schwartz, 1997;Borden, 1998;Pfeffer et al, 1998;Borden et al, 2000) Although IFNa (type I) and IFNg (type II) shared common biological properties, signal transduction of IFNg and IFNa involves both similar and dissimilar pathways.…”

Section: Introductionmentioning

confidence: 99%

“…As IFNg has been shown to increase the sensitivity of many cells to various apoptotic stimuli (Suk et al, 2001a;Chawla-Sarkar et al, 2003), we investigated whether IFNg acts in synergy with either IFNa or TNFa to induce apoptosis of SK-N-MC cells. In the present work we demonstrate that although IFNa and TNFa alone are unable to induce cell death, they act in synergy with IFNg to induce SK-N-MC cell death.…”

Section: Introductionmentioning

confidence: 99%

Type I interferon and TNFα cooperate with type II interferon for TRAIL induction and triggering of apoptosis in SK-N-MC EWING tumor cells

Abadie

Besançon

2004

Oncogene

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Ewing's sarcoma is the second most common human bone tumor in childhood. Here, we investigated the sensitivity of the Ewing tumor cell line, SK-N-MC, to the apoptotic effect of type I (IFNa) and type II (IFNc) interferons and TNFa. We demonstrate that although IFNa and TNFa alone are unable to induce cell death, they act in synergy with IFNc to induce SK-N-MC cell apoptosis. The synergistic induction of apoptosis correlated with the synergistic induction of TNFa-related apoptosis-inducing ligand (TRAIL) mRNA and TRAIL protein synthesis as well as of TRAIL secretion. Preparations of inducer-free supernatants from SK-N-MC cells stimulated with combinations of cytokines were shown to be cytotoxic for untreated SK-N-MC cells. This cytotoxicity was partially inhibited by addition of TRAILR2/Fc fusion protein, indicating that the secreted TRAIL mediates, at least in part, the apoptotic effect displayed by the supernatants of stimulated SK-N-MC cells. We have shown that the presence of IFNc is required to allow the sustained expression of IRF1 in SK-N-MC cells stimulated by addition of IFNa or TNFa suggesting that IRF1 plays a role in the synergistic induction of apoptosis by combinations of cytokines. Furthermore, we have shown that inhibition of NF-jB activation contributes to the IFNc-mediated sensitization to the apoptotic effect of TNFa. To our knowledge, this is the first report showing that interferon/cytokine combinations are able to induce TRAIL gene expression and TRAIL protein synthesis and secretion in Ewing sarcoma-derived cells. We believe that the observations reported here might contribute to the development of alternative new approaches to the treatment of Ewing tumors resistant to conventional therapy.

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Cited by 732 publications

References 91 publications

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

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

Interferon-regulatory factor-1 is critical for tamoxifen-mediated apoptosis in human mammary epithelial cells

Type I interferon and TNFα cooperate with type II interferon for TRAIL induction and triggering of apoptosis in SK-N-MC EWING tumor cells

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