Early work on the function of CD95, an interview with Shige Nagata

Nagata, Shinji

doi:10.1038/sj.cdd.4401453

Cited by 10 publications

(11 citation statements)

References 28 publications

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“…Molecular mechanisms of this problem are still unknown and are the subject of many studies [14,15,16]. One of those mechanisms is the Fas/FasL system, which has been studied for many years [1,2,25]. The Fas/FasL system induces cell death pathway via receptors (extrinsic pathway).…”

Section: Discussionmentioning

confidence: 99%

“…Many inducers and inhibitors of this way of apoptosis have been reported. It is well recognized that the Fas/FasL pathway is involved in the apoptotic process in different pathologies and in the cytotoxic effects of most immuno-and chemotherapeutic agents [1,2,26,27]. The expression and function of the Fas receptor play an important role in the maintaining of homeostasis.…”

Section: Discussionmentioning

confidence: 99%

“…Fas was the first death receptor to be described as an apoptosis-inducing receptor [1]. FasL (CD95L, APO-1L) is expressed on activated T cells and NK cells, and mediates immune responses [2]. Membrane-bound FasL induces apoptotic cell death of Fas-positive cells [3].…”

Section: Introductionmentioning

confidence: 99%

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Fas and FasL expression on cells of two transplantable melanoma lines according to their different biological properties.

Zielińska

Kozłowska²,

Cichorek³

et al. 2008

Folia Histochem Cytobiol.

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Abstract. Fas and FasL interaction induces apoptotic cell death. In immunocompetent cells it plays a crucial role in the effector functions of the cells and in the regulation of host immune response. In tumours (e.g. melanoma), FasL expression possibly counteracts the Fas-positive effector T cells that infiltrate into tumours, and consequently the Fas/FasL interaction can contribute to the escape of tumour cells from the systemic immune response. In this study we examined differences in Fas and FasL expression on cells from the hamster melanotic melanoma line (Ma) and a more aggressive amelanotic melanoma line (Ab). We also tried to find out whether the Fas/FasL expression induces an ability to undergo spontaneous apoptosis in these two transplantable melanoma lines. Our previous studies have shown that cells of the Ma line have a higher ability to undergo spontaneous apoptosis than cells of the Ab line. Isolated transplantable melanoma cells were incubated for 4 and 24 hours and after that time the expression of Fas and FasL was estimated by flow cytometry. The results show that there was no Fas expression, although FasL was detected on both melanoma cell lines. Therefore the data reported by other authors indicate that a lack or a low level of Fas expression and an ectopic expression of FasL on melanoma cells can be an escape mechanism of the tumour, to avoid host immune responses. The content of FasL-positive melanotic melanoma cells was higher than in amelanotic melanoma cells and increased with the prolongation of the incubation time. FasL expression on amelanotic melanoma cells was detected after 24 hours at a level similar to that on melanotic melanoma cells after 4 hours incubation time. FasL expression on melanoma cells can induce apoptosis in cytotoxic T lymphocytes and NK cells which are responsible for tumour cells elimination. The results obtained suggest that the Fas/FasL system does not play any significant role in spontaneous apoptosis of two melanoma cell lines. But these results may indicate the presence of immune privilege of tumour cells with FasL expression.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Fas and FasL expression on cells of two transplantable melanoma lines according to their different biological properties.

Zielińska

Kozłowska²,

Cichorek³

et al. 2008

Folia Histochem Cytobiol.

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“…The lethal effect of chemotherapeutic drugs upon tumour cells is achieved primarily through the induction of apoptosis. Among the numerous signalling pathways that regulate apoptosis is the Fas/FasL pathway (Walczak and Krammer, 2000; Nagata, 2004). Fas (Apo‐1, CD95), a type I cell membrane glycoprotein belonging to the TNFR (tumour necrosis factor receptor) superfamily, transmits specific ligand‐induced apoptotic signals and directs apoptotic processes (Bullani et al, 2002).…”

Section: Introductionmentioning

confidence: 99%

PEG‐liposomal oxaliplatin induces apoptosis in human colorectal cancer cells via Fas/FasL and caspase‐8

Yang

Liu

2012

Cell Biology International

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Since cellular uptake of PEG [poly(ethylene glycol)]-liposomal L-OHP (oxaliplatin) induces bioactive changes in CRC (colorectal cancer), we have investigated its apoptotic effect and anticancer mechanism. Human CRC SW480 cells were treated with PEG-liposomal L-OHP and a caspase-8 inhibitor [Z-IETD-FMK (benzyloxycarbonyl-Ile-Glu-Thr-dl-Asp-fluoromethylketone)]. Apoptosis was measured by FCM (flow cytometry) and TUNEL (terminal deoxynucleotidyl transferase-mediated dUTP nick-end labelling) assay. Expression of Fas/FasL and cytochrome c was detected using FCM and an immunofluorescence assay. Expression of caspase-8, Bid, caspase-9, caspase-7 and activated caspase-3 (P17) was examined by Western blot analyses. The results indicated that PEG-liposomal L-OHP (28 μg/ml L-OHP) induced marked apoptosis in SW480 cells compared with 28 μg/ml free L-OHP. The expression levels of Fas, FasL, cytochrome c, caspase-9, caspase-7 and activated caspase-3 proteins were up-regulated, with a corresponding increase in apoptosis; however, expression of caspase-8 and Bid were down-regulated as apoptosis increased. When cells were treated with Z-IETD-FMK, apoptosis was inhibited, but there was little impact on the expression of Fas, FasL, cytochrome c, Bid, caspase-9, caspase-7 and activated caspase-3. These findings indicate that PEG-liposomal L-OHP enhances the anticancer potency of the chemotherapeutic agent; moreover, Fas/FasL and caspase-8 signalling pathways play a key role in mediating PEG-liposomal L-OHP-induced apoptosis.

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“…As described by Nagata in a 2004 interview, he usually tried to map the loci of genes cloned in the lab to see if there was any relevance to disease (6). Collaborators Nancy Jenkins and Neal Copeland at NIH mapped the mouse Fas locus to a location on chromosome 19, close to where the lpr locus had previously been mapped (7).…”

mentioning

confidence: 99%