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University Feinberg School of Medicine"],"full_dataset_link":["https://www.ebi.ac.uk/ena/browser/view/PRJNA393938"],"scientific_name":["Homo sapiens"],"long_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. Overall design: 293T (shL3 site deleted) cells were infected with either pTIP-shScr or pTIP-shL3 and following puromycin selection large RNAs were analyzed by deep sequencing 50 or 100hrs after addition of doxycycline/HeyA8 (shR6 site deleted) cells were infected with either pLKO-shScr or pLKO-shR6 and following puromycin selection large RNAs were analyzed by deep sequencing 50 or 100hrs after addition of selection."],"tag":["xref:PubMed:29063830"],"repository":["ENA"],"name_synonyms":["Human, Modern., human being, Man (Taxonomy), Homo sapiens, man, Man, human, Modern Man"],"description_synonyms":["Tumor Necrosis Factor Ligand Superfamily Member 6, post-transcriptional gene silencing by RNA, RNA, Materials, Malignant Neoplasm, CD178 Antigens, Neoplasms, CD95-L, Benign Neoplasm, posttranscriptional gene silencing by siRNA, Gene, Tumor, cosuppression, Malignant, Cistrons, Cell, CD178, gld, ALPS1B, Antigens, Tnfsf6, RNAi, MT, Benign, Interference, survival, Antigen, Neoplasm, Post Transcriptional, CD95 Antigen Ligand, Genetic Materials, RNA Silencing, Silencing, Post-Transcriptional Gene, Fas-L, Post-Transcriptional Gene Silencings, primary cancer, Genetic, death rate, Malignancy, Fas Ligand, Posttranscriptional, Posttranscriptional Gene Silencing, Fas Ligand (FasL), Benign Neoplasms, CD95 Ligand, Cancers, Co Suppression, quelling, CD178 Antigen, Cosuppression, TNF Superfamily, malignant tumor, Post Transcriptional Gene Silencing, Malignant Neoplasms, CD95L, Neoplasias, Gene Silencings, APT1LG1, Post-Transcriptional, Gene Silencing, malignant neoplasm, Material, FasL Protein, time of survival, Cistron, FASL, TNFSF6, Member 6, Malignancies, Genetic Material., Co-Suppression, APTL, Post-Transcriptional Gene Silencing, Faslg, Neoplasia, Cancer, Tumors"],"additional_accession":[]},"is_claimable":false,"name":"Homo sapiens","description":"CD95L derived si- and shRNAs kill cancer cells through an RNAi mechanism by targeting survival genes [shL3.shR6.RNAseq.lg]","dates":{"last_updated":"2025-09-24","first_public":"2017-09-18"},"accession":"PRJNA393938","cross_references":{"GEO":["GSE101234"],"taxon":["9606"],"PubMed":["29063830"]}}