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CD95L derived si- and shRNAs kill cancer cells through an RNAi mechanism by targeting survival genes

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Homo sapiens

PROVIDER: GSE87817 | GEO | 2017/09/16

SECONDARY ACCESSION(S): PRJNA347649

REPOSITORIES: GEO

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CD95L derived si- and shRNAs kill cancer cells through an RNAi mechanism by targeting survival genes [AGOpulldownRNAseq.sm]

Project description:>80% of a large number of tested siRNAs and shRNAs targeting CD95 or CD95 ligand (CD95L) induce a form of cell death that is characterized by the simultaneous activation of multiple death pathways and preferentially affects transformed and cancer stem cells. We now show that these si/shRNAs kill cancer cells through canonical RNAi by targeting the 3’UTR of critical survival genes in a unique form of off-target effect. We also provide evidence showing that the full length CD95L mRNA is also toxic and produces small Ago-associated RNAs.

2017-09-16 | GSE101166 | GEO

CD95L derived si- and shRNAs kill cancer cells through an RNAi mechanism by targeting survival genes [FasLRNAseq.lg]

2017-09-16 | GSE101232 | GEO

CD95L derived si- and shRNAs kill cancer cells through an RNAi mechanism by targeting survival genes [shL1.RNAseq.lg]

Project description:We provide evidence that shRNAs and siRNAs derived from CD95 and CD95L preferentially target the 3' UTRs of survival genes culminating in a very robust mode of cell death we call DISE (Death Induced by Survival gene Elimination)

2017-09-16 | GSE101157 | GEO

CD95L derived si- and shRNAs kill cancer cells through an RNAi mechanism by targeting survival genes [shL3.shR6.RNAseq.lg]

Project description:The death receptor CD95/Fas can be activated by immune cells to kill cancer cells. However, most siRNAs or shRNAs targeting either CD95 or CD95L induce DICE (Death Induced by CD95/CD95L Elimination), a form of cell death in which a combination of different cell death pathways are activated, that is selective for transformed cells, and that preferentially affects cancer stem cells. We now provide evidence that both CD95 and CD95L are part of a network of genes that contain sequences that when expressed as either siRNAs or shRNAs are toxic to cancer cells. They act through canonical RNAi by targeting the 3'UTRs of critical survival genes. We propose that these embedded toxic sequences are part of a conserved mechanism that regulates cell death, and we predict the existence of endogenous siRNAs, that when produced, induce cell death to regulate genome fidelity. Our data have implications for cancer therapy and the use of RNAi.

2017-09-16 | GSE101234 | GEO

CD95L derived si- and shRNAs kill cancer cells through an RNAi mechanism by targeting survival genes [shL3.shR6.RNAseq.sm]

2017-09-16 | GSE101183 | GEO

CD95L derived si- and shRNAs and the CD95L mRNA kill cancer cells through an RNAi mechanism by targeting survival genes [siL3.RNAseq.lg]

2017-09-16 | GSE101167 | GEO

CD95L derived si- and shRNAs kill cancer cells through an RNAi mechanism by targeting survival genes

Project description:CD95L derived si- and shRNAs kill cancer cells through an RNAi mechanism by targeting survival genes

| PRJNA347649 | ENA

Many si/shRNAs can kill cancer cells by targeting multiple survival genes through an off-target mechanism.

Project description:Over 80% of multiple-tested siRNAs and shRNAs targeting CD95 or CD95 ligand (CD95L) induce a form of cell death characterized by simultaneous activation of multiple cell death pathways preferentially killing transformed and cancer stem cells. We now show these si/shRNAs kill cancer cells through canonical RNAi by targeting the 3'UTR of critical survival genes in a unique form of off-target effect we call DISE (death induced by survival gene elimination). Drosha and Dicer-deficient cells, devoid of most miRNAs, are hypersensitive to DISE, suggesting cellular miRNAs protect cells from this form of cell death. By testing 4666 shRNAs derived from the CD95 and CD95L mRNA sequences and an unrelated control gene, Venus, we have identified many toxic sequences - most of them located in the open reading frame of CD95L. We propose that specific toxic RNAi-active sequences present in the genome can kill cancer cells.

| S-EPMC5655136 | biostudies-literature

TMEFF2 and CD95L derived shRNAs promote prostate cancer cell death by targeting the essential androgen receptor pathway

Project description:A novel mechanism, Death Induced by Survival gene Elimination (DISE), has recently been described as a potential cancer therapy. DISE kills cancer cells through an RNA interference (RNAi) mechanism. We show that expression of certain shRNAs developed to target TMEFF2 promotes prostate cancer (PCa) cell death similar to DISE, and independently of TMEFF2 targeting/expression. In PCa cells, these shRNAs downregulate the androgen receptor (AR) and AR coregulatory genes, an effect that correlates with the presence of short seed matches in their 3’UTRs and which results in global androgen signaling inhibition and cell death. We have termed this mechanism Androgen Network DISE (AN-DISE). shL3, an shRNA to CD95L known to promote DISE in non-PCa cells, promotes AN-DISE in PCa cells by targeting the AR-signaling pathway.

2021-02-01 | GSE165247 | GEO

CD95/Fas suppresses NF-κB activation through recruitment of KPC2 in a CD95L/FasL-independent mechanism.

Project description:CD95 expression is preserved in triple-negative breast cancers (TNBCs), and CD95 loss in these cells triggers the induction of a pro-inflammatory program, promoting the recruitment of cytotoxic NK cells impairing tumor growth. Herein, we identify a novel interaction partner of CD95, Kip1 ubiquitination-promoting complex protein 2 (KPC2), using an unbiased proteomic approach. Independently of CD95L, CD95/KPC2 interaction contributes to the partial degradation of p105 (NF-κB1) and the subsequent generation of p50 homodimers, which transcriptionally represses NF-κB-driven gene expression. Mechanistically, KPC2 interacts with the C-terminal region of CD95 and serves as an adaptor to recruit RelA (p65) and KPC1, which acts as E3 ubiquitin-protein ligase promoting the degradation of p105 into p50. Loss of CD95 in TNBC cells releases KPC2, limiting the formation of the NF-κB inhibitory homodimer complex (p50/p50), promoting NF-κB activation and the production of pro-inflammatory cytokines, which might contribute to remodeling the immune landscape in TNBC cells.

| S-EPMC8666665 | biostudies-literature

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