CD95 is a key mediator of invasion and accelerated outgrowth of mouse colorectal liver metastases following radiofrequency ablation

Nijkamp, Maarten W.; Hoogwater, Frederik J.H.; Steller, Ernst J.A.; Westendorp, B. Florien; Meulen, Taco A. van der; Leenders, M.W.H.; Rinkes, Inne H.M. Borel; Kranenburg, Onno

doi:10.1016/j.jhep.2010.04.040

Cited by 51 publications

(41 citation statements)

References 40 publications

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“…Fas) or other proteins in the death receptor pathways (e.g. caspase-8 and Fas-associated death domain) promotes tumor formation, growth, invasion, and even metastasis (45)(46)(47)(48)(49)(50)(51)(52). Thus, it is also possible that Ras-induced DR5 expression is involved in promoting Ras-mediated oncogenesis and/or metastasis, particularly under apoptosis-compromised conditions.…”

Section: Discussionmentioning

confidence: 99%

Oncogenic Ras and B-Raf Proteins Positively Regulate Death Receptor 5 Expression through Co-activation of ERK and JNK Signaling

Yue

Zhou

et al. 2012

Journal of Biological Chemistry

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Background:The oncogene Ras induces DR5 expression with undefined mechanism. Results: Both Ras and B-Raf induce DR5 expression through co-activation of ERK and JNK signaling and subsequent cooperative effects among CHOP, Elk1, and c-Jun. Conclusion: Co-activation of ERK and JNK signaling accounts for Ras-induced DR5 expression. Significance: A novel function of DR5 in Ras-or B-Raf-mediated oncogenesis may be suggested.

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Section: Discussionmentioning

confidence: 99%

Oncogenic Ras and B-Raf Proteins Positively Regulate Death Receptor 5 Expression through Co-activation of ERK and JNK Signaling

Yue

Zhou

et al. 2012

Journal of Biological Chemistry

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“…Although Fas signaling was reported to induce tumor apoptosis and inhibit tumor growth in vivo when triggered by FasL (5)(6)(7), accumulated evidence also demonstrated that, in the presence of certain levels of FasL, Fas signaling promotes, not inhibits, tumor growth in Fas-resistant tumor cells (8,9). In addition to inducing tumor cell proliferation, Fas ligation was proved to advance cell cycle and increase tumor motility and invasiveness (10)(11)(12)(13)(14). All of these studies suggest that Fas signaling plays an important role in tumor progress in Fas-resistant tumors.…”

mentioning

confidence: 99%

Activated T Cell Exosomes Promote Tumor Invasion via Fas Signaling Pathway

Cai

Yang

et al. 2012

The Journal of Immunology

233

174

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Activated T cells release bioactive Fas ligand (FasL) in exosomes, which subsequently induce self-apoptosis of T cells. However, their potential effects on cell apoptosis in tumors are still unknown. In this study, we purified exosomes expressing FasL from activated CD8+ T cell from OT-I mice and found that activated T cell exosomes had little effect on apoptosis and proliferation of tumor cells but promoted the invasion of B16 and 3LL cancer cells in vitro via the Fas/FasL pathway. Activated T cell exosomes increased the amount of cellular FLICE inhibitory proteins and subsequently activated the ERK and NF-κB pathways, which subsequently increased MMP9 expression in the B16 murine melanoma cells. In a tumor-invasive model in vivo, we observed that the activated T cell exosomes promoted the migration of B16 tumor cells to lung. Interestingly, pretreatment with FasL mAb significantly reduced the migration of B16 tumor cells to lung. Furthermore, CD8 and FasL double-positive exosomes from tumor mice, but not normal mice, also increased the expression of MMP9 and promoted the invasive ability of B16 murine melanoma and 3LL lung cancer cells. In conclusion, our results indicate that activated T cell exosomes promote melanoma and lung cancer cell metastasis by increasing the expression of MMP9 via Fas signaling, revealing a new mechanism of tumor immune escape.

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“…18 The expression of CD95 on cancer cells suggests that cancer cells maintain CD95 expression for activities other than apoptosis induction. Consistent with this assumption are data demonstrating roles for CD95 in promoting cancer cell migration, growth, epithelial-to-mesenchymal transition (EMT), and development, as shown in lung cancer, 19,20 colon cancer, [21][22][23][24] gastrointestinal cancers, 25,26 pancreatic cancer, 27,28 glioblastoma multiforme (GBM), 29 and in 22 cell lines representing various cancers. 30 Our most recent finding is that cancer fails to develop in mouse models of low-grade or endometrioid ovarian cancer or liver cancer unless CD95 is expressed, 14,31 suggesting that the reason cancer cells usually express CD95 goes beyond a function of CD95 as a tumor promoter.…”

Section: Nonapoptotic Signaling Through Cd95 In Normal Cells and In Cmentioning

confidence: 66%

Dice

Marynen

2014

Cell Cycle

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CD95 is a key mediator of invasion and accelerated outgrowth of mouse colorectal liver metastases following radiofrequency ablation

Cited by 51 publications

References 40 publications

Oncogenic Ras and B-Raf Proteins Positively Regulate Death Receptor 5 Expression through Co-activation of ERK and JNK Signaling

Oncogenic Ras and B-Raf Proteins Positively Regulate Death Receptor 5 Expression through Co-activation of ERK and JNK Signaling

Activated T Cell Exosomes Promote Tumor Invasion via Fas Signaling Pathway

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