Erratum: The role of CD95 and CD95 ligand in cancer

Peter, Marcus E.; Hadji, Abbas; Murmann, Andrea E.; Brockway, Sonia; Putzbach, William; Pattanayak, Abhinandan; Ceppi, Paolo

doi:10.1038/cdd.2015.25

Cited by 68 publications

(41 citation statements)

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“…CD95 possesses tumor promoting activities (Peter et al, 2015). We recently demonstrated that chronic stimulation of CD95 increases and maintains cancer stemness (Ceppi et al, 2014).…”

Section: Discussionmentioning

confidence: 99%

“…CD95 (APO-1/Fas) is an apoptosis-inducing death receptor but also has multiple nonapoptotic and tumor promoting activities (Peter et al, 2015). Stimulation of CD95 increases migration of multiple cancer cells (Barnhart et al, 2004; Kleber et al, 2008).…”

Section: Introductionmentioning

confidence: 99%

“…CD95 couples to multiple signaling pathways, which all contribute to CD95’s nonapoptotic activities. These include MAP kinases, NF-κB, Scr kinases, and PI3K (reviewed in (Peter et al, 2015)). Activation of all these pathways are detectable within a few hours following CD95 stimulation.…”

Section: Introductionmentioning

confidence: 99%

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CD95/Fas Increases Stemness in Cancer Cells by Inducing a STAT1-Dependent Type I Interferon Response

et al. 2017

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SUMMARY Stimulation of CD95/Fas drives and maintains cancer stem cells (CSCs). We now report that this involves activation of STAT1, induction of STAT1 regulated genes, and this process is inhibited by active caspases. STAT1 is enriched in CSCs in cancer cell lines, patient-derived human breast cancer, and CD95high expressing glioblastoma neurospheres. CD95 stimulation of cancer cells induced secretion of Type I interferons (IFNs) that bind to Type I IFN receptors, resulting in activation of JAK kinases, activation of STAT1, and induction of a number of STAT1-regulated genes that are part of a gene signature recently linked to therapy resistance in 5 primary human cancers. Consequently, we identified Type I IFNs as drivers of cancer stemness. Knockdown or knock-out of STAT1 resulted in a strongly reduced ability of CD95L or type I IFN to increase cancer stemness. This identifies STAT1 as a key regulator of the CSC-inducing activity of CD95.

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“…CD95 possesses tumor promoting activities (Peter et al, 2015). We recently demonstrated that chronic stimulation of CD95 increases and maintains cancer stemness (Ceppi et al, 2014).…”

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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CD95/Fas Increases Stemness in Cancer Cells by Inducing a STAT1-Dependent Type I Interferon Response

et al. 2017

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“…Downregulation of Fas expression has been implicated in tumor progression in various types of cancer, including gastric, ovarian, lung and renal carcinoma (5,14–18), and has been hypothesized to result in reduced tumor apoptosis (19–26). The present study revealed that Fas expression was correlated with caspase-8, caspase-3 and PARP1 expression in the gastric cancer tissues and cell lines.…”

Section: Discussionmentioning

confidence: 99%

Fas expression is downregulated in gastric cancer

Wang

Chen

et al. 2016

Molecular Medicine Reports

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The aim of the present study was to investigate Fas expression in tumor samples from patients with gastric cancer, in order to determine the involvement of the Fas signaling pathway. The protein expression levels of Fas, caspase-8, caspase-3 and poly (adenosine diphosphate-ribose) polymerase 1 (PARP1) were examined in gastric cancer specimens and their associations with clinical pathological parameters were analyzed with immunohistochemical staining and western blot analysis. The mRNA expression was quantified with quantitative PCR and apoptosis was examined with a FACScan flow cytometer. The results demonstrated that the downregulation of Fas expression was correlated with less histological differentiation, gender (male), and increased lymph node and distant metastases (P<0.05). In the AGS established gastric cancer cell line, upregulation of the Fas signaling pathway promoted the apoptosis of gastric cancer cells by upregulating the expression of caspase-8 and caspase-3, and downregulating the expression of PARP1. The present study demonstrated that Fas was associated with gastric cancer and promoted the apoptosis of gastric cancer cells via caspase-8, caspase-3 and PARP1. These results suggested that caspase-8, caspase-3 and PARP1 may be triggers of gastric cancer, and upregulation of caspase-8 and caspase-3 expression, or inhibition of PARP1 expression may improve the therapeutic outcome in patients with gastric cancer.

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“…Fetal trophoblasts also express the inhibitory molecule CD95L (Fas ligand), a protein ordinarily expressed in activated T cells but constitutively expressed in immune‐privileged sites, which induces apoptosis in CD95 (Fas)‐expressing cytotoxic lymphocytes . Cancer cells express both Fas and Fas ligand, and are generally resistant to this path of apoptotic death . This is achieved either through altered expression of Fas or co‐expression of a protein that prevents correct assemblage of the death‐inducing signaling complex (DISC), and is an important mechanism of treatment‐resistance …”

Section: Placental Reproduction Relies On Maternal Tolerance Of the Fmentioning

confidence: 99%

Understanding Immune Tolerance of Cancer: Re‐Purposing Insights from Fetal Allografts and Microbes

et al. 2018

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Cancer cells seem to exploit mechanisms that evolve as part of physiological tolerance, which is a complementary and often beneficial form of defense. The study of physiological systems of tolerance can therefore provide insights into the development of a state of host tolerance of cancer, and how to break it. Analysis of these models has the potential to improve our understanding of existing immunological therapeutic targets, and help to identify future targets and rational therapeutic combinations. The treatment of cancer with immune checkpoint inhibitors aims to reverse the progression to tolerance of cancer, and achieve an immunogenic, rather than tolerogenic, homeostasis. Broadening the efficacy and durability of checkpoint inhibitors focuses on reversing tolerance and stimulating immunogenicity in the cancer, host, and environment. Two examples of important physiological states of tolerance that may inform tolerance of cancer are microbial infection and placental reproduction. These states of tolerance result from bilateral shaping of host and non-self, akin to immunoediting in cancer, and offer reliable models to study the immune tolerance paradigm.

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Erratum: The role of CD95 and CD95 ligand in cancer

Cited by 68 publications

References 0 publications

CD95/Fas Increases Stemness in Cancer Cells by Inducing a STAT1-Dependent Type I Interferon Response

CD95/Fas Increases Stemness in Cancer Cells by Inducing a STAT1-Dependent Type I Interferon Response

Fas expression is downregulated in gastric cancer

Understanding Immune Tolerance of Cancer: Re‐Purposing Insights from Fetal Allografts and Microbes

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