Fas antigen signals proliferation of normal human diploid fibroblast and its mechanism is different from tumor necrosis factor receptor

Aggarwal, Bharat B.; Singh, Sanjaya; LaPushin, Ruth; Tótpál, Klára

doi:10.1016/0014-5793(95)00339-b

Cited by 130 publications

(77 citation statements)

References 16 publications

(21 reference statements)

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“…Although usually associated with induction of apoptosis, Fas has been shown to be capable of transducing a proliferative signal in human fibroblasts. 45 Further, different cell types can utilise different pathways downstream of Fas. Type I cells are characterised by rapid activation of caspase-8 and caspase-3 with strong induction of the death-inducing signalling complex (DISC).…”

Section: Cell Death and Differentiationmentioning

confidence: 99%

Fas-independent apoptosis in T-cell tumours induced by the CD2-myc transgene

Cameron¹,

Morton²,

Johnston³

et al. 2000

Cell Death Differ

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Depending on the cellular context, the Myc oncoprotein is capable of promoting cell proliferation or death by apoptosis. These observations suggest that apoptosis in response to deregulated gene expression may represent a natural brake to tumour development. The pathways by which Myc induces apoptosis are as yet poorly characterised although recent observations on rat fibroblasts over-expressing Myc have demonstrated a requirement for the Fas pathway. To investigate the role of Fas in Myc-induced lymphomagenesis we backcrossed CD2-myc mice onto an lpr background. Rates of tumour development and phenotypic properties, including levels of apoptosis were indistinguishable from CD2-myc controls. Further, tumour cell lines derived from mice expressing a regulatable form of Myc showed inducible apoptosis at similar rates regardless of their lpr genotype. These results show that activation of c-myc and loss of Fas do not collaborate in T lymphoma development and that Mycinduced apoptosis in T-cells occurs by Fas-independent pathways. Cell Death and Differentiation (2000) 7, 80 ± 88.

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Section: Cell Death and Differentiationmentioning

confidence: 99%

Fas-independent apoptosis in T-cell tumours induced by the CD2-myc transgene

Cameron¹,

Morton²,

Johnston³

et al. 2000

Cell Death Differ

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“…Treatment of cells with TNF-a or activation of the Fas receptor induces apoptosis (Itoh et al, 1991;Nagata and Golstein, 1995;Tartaglia et al, 1993a;Trauth, et al, 1989), although some exceptions have been reported (Aggarwal et al, 1995;Alderson et al, 1993). Cells express two distinct TNF-a receptors and the p55 TNF receptor is thought to be responsible for signaling TNF-ainduced cytotoxicity (Tartaglia et al, 1991(Tartaglia et al, , 1993aThoma et al, 1990).…”

Section: Introductionmentioning

confidence: 99%

“…Since Fas and p55 TNF receptor require a conserved sequence motif to signal cell death, it is possible they share signal transduction components (Itoh and Nagata, 1993;Tartaglia et al, 1993b). However, several reports have suggested that Fas and TNF receptor signaling pathways are distinct (Aggarwal et al, 1995;Grell et al, 1994;Hug et al, 1994, Nagata andGolstein, 1995;Sato et al, 1995, Schulze-Osthoff et al, 1994Wong and Goeddel, 1994;Zimmerman et al, 1989). In particular, stimulation of a fibrosarcoma cell line engineered to ectopically express the Fas receptor does not lead to activation of NF-kB, yet NF-kB is induced when these cells are treated with TNF-a (Schulze-Osthoff et al, 1994).…”

Section: Introductionmentioning

confidence: 99%

Fas activates NF-κB and induces apoptosis in T-cell lines by signaling pathways distinct from those induced by TNF-α

et al. 1997

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The p55 tumor necrosis factor (TNF) receptor and the Fas (CD95/APO-1) receptor share an intracellular domain necessary to induce apoptosis, suggesting they utilize common signaling pathways. To define pathways triggered by Fas and TNF-a we utilized human CEM-C7 T-cells. As expected, stimulation of either receptor induced apoptosis and TNF-ainduced signaling included the activation of NF-kB. Surprisingly, Fas-induced signaling also triggered the activation of NF-kB in T cells, yet the kinetics of NF-kB induction by Fas was markedly delayed. NF-kB activation by both pathways was persistent and due to the sequential degradation of IkB-a and IkB-b. However, the kinetics of IkB degradation were different and there were differential effects of protease inhibitors and antioxidants on NF-kB activation. Signaling pathways leading to activation of apoptosis were similarly separable and were also independent of NF-kB activation. Thus, the Fas and TNF receptors utilize distinct signal transduction pathways in Tcells to induce NF-kB and apoptosis.

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“…However, the mere presence of these CD95/Fas signalling components does not prove the existence of an active extrinsic death pathway. Moreover, many Fas-expressing cells do not undergo death when Fas receptor is bound by its ligand, 15 and alternative biological processes such as proliferation in T cells 16 and fibroblasts, 17 activation of NFkB 18 and neurite formation in primary sensory neurones 19 have been attributed to Fas ligation.…”

mentioning

confidence: 99%