|
| Status |
Public on Sep 16, 2017 |
| Title |
CD95L derived si- and shRNAs kill cancer cells through an RNAi mechanism by targeting survival genes [FasLRNAseq.lg] |
| Organism |
Homo sapiens |
| Experiment type |
Expression profiling by high throughput sequencing
|
| Summary |
>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.
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| |
|
| Overall design |
Examination of differential gene mRNA expression in empty vector control cells versus cells over-expressing CD95L mRNA.
|
| |
|
| Contributor(s) |
Putzbach W, Peter ME, Bartom E |
| Citation(s) |
29063830 |
| NIH grant(s) |
| Grant ID |
Grant title |
Affiliation |
Name |
| R35 CA197450 |
DISE - a natural cancer surveillance mechanism - a new road to cancer therapy |
NORTHWESTERN UNIVERSITY AT CHICAGO |
Marcus E. Peter |
|
| |
| Submission date |
Jul 11, 2017 |
| Last update date |
Sep 08, 2022 |
| Contact name |
Marcus Peter |
| E-mail(s) |
[email protected]
|
| Organization name |
Northwestern University Feinberg School of Medicine
|
| Street address |
303 East Superior Street, Lurie 6-123
|
| City |
Chicago |
| State/province |
IL |
| ZIP/Postal code |
60611 |
| Country |
USA |
| |
|
| Platforms (1) |
| GPL20301 |
Illumina HiSeq 4000 (Homo sapiens) |
|
| Samples (4)
|
| GSM2700503 |
503 HeyA8 KO C11 pLenti 50hrs (rep 1, lg) |
| GSM2700504 |
04 HeyA8 KO C11 pLenti 50hrs (rep 2, lg) |
| GSM2700505 |
505 HeyA8 KO C11 FasL 50hrs (rep 1, lg) |
| GSM2700506 |
506 HeyA8 KO C11 FasL 50hrs (rep 2, lg) |
|
| This SubSeries is part of SuperSeries: |
| GSE87817 |
CD95L derived si- and shRNAs kill cancer cells through an RNAi mechanism by targeting survival genes |
|
| Relations |
| BioProject |
PRJNA393897 |
| SRA |
SRP111577 |
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