ArticleBlood2013
RNAi screening uncovers Dhx9 as a modifier of ABT-737 resistance in an Eμ-myc/Bcl-2 mouse model.
Article in Blood, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
24 citing papers in PubMed, 31 citations in OpenAlex.
- Cytosolic Nuclear Sensor Dhx9 Controls Medullary Thymic Epithelial Cell Differentiation by p53-Mediated Pathways.Frontiers in immunology · 2022Article
- DHX9 contributes to the malignant phenotypes of colorectal cancer via activating NF-κB signaling pathway.Cellular and molecular life sciences : CMLS · 2021Article
- The enigmatic helicase DHX9 and its association with the hallmarks of cancer.Future science OA · 2020Review
- Article
- A DHX9-lncRNA-MDM2 interaction regulates cell invasion and angiogenesis of cervical cancer.Cell death and differentiation · 2019Article
- Genome-wide prediction of synthetic rescue mediators of resistance to targeted and immunotherapy.Molecular systems biology · 2019Article
- The sequence features that define efficient and specific hAGO2-dependent miRNA silencing guides.Nucleic acids research · 2018Article
- Polysome-profiling in small tissue samples.Nucleic acids research · 2018Article
- Nol12 is a multifunctional RNA binding protein at the nexus of RNA and DNA metabolism.Nucleic acids research · 2017Article
- Suppression of Transposable Elements in Leukemic Stem Cells.Scientific reports · 2017Article
- Nucleic acid sensing pattern recognition receptors in the development of colorectal cancer and colitis.Cellular and molecular life sciences : CMLS · 2017Review
- Dependence of p53-deficient cells on the DHX9 DExH-box helicase.Oncotarget · 2017Article
- RNA helicase DHX9 may be a therapeutic target in lung cancer and inhibited by enoxacin.American journal of translational research · 2017Article
- DHX33 Transcriptionally Controls Genes Involved in the Cell Cycle.Molecular and cellular biology · 2016Article
- The mitochondrial translation machinery as a therapeutic target in Myc-driven lymphomas.Oncotarget · 2016Article
- Article
- The biology of DHX9 and its potential as a therapeutic target.Oncotarget · 2016Review
- The RNA helicase A in malignant transformation.Oncotarget · 2016Review
- Repression of p53-target gene Bbc3/PUMA by MYSM1 is essential for the survival of hematopoietic multipotent progenitors and contributes to stem cell maintenance.Cell death and differentiation · 2016Article
- Genotoxic stress inhibits Ewing sarcoma cell growth by modulating alternative pre-mRNA processing of the RNA helicase DHX9.Oncotarget · 2015Article
Corrections and comments
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Authors and funding
11 authors at 6 institutions in 4 countries.
Funding
Abstract
ABT-737 is a promising chemotherapeutic agent that promotes apoptosis by acting as a selective BH3 mimetic to neutralize Bcl-2-like family members. One shortcoming with its use is that Mcl-1, a member of the Bcl-2 family, is poorly inhibited by ABT-737 and thus is a major cause of resistance. We performed a short hairpin RNA (shRNA)-based drop-out screen to identify novel genes and pathways that could reverse resistance to ABT-737 treatment in Eµ-myc/Bcl-2 lymphoma cells engineered to rely on endogenous Mcl-1 for survival. Several drug-sensitive shRNAs were identified that were selectively depleted in the presence of ABT-737. Of these, 2 independent shRNAs targeting the RNA/DNA helicase Dhx9 were found to sensitize lymphomas to ABT-737 to an extent comparable to control Mcl-1 shRNAs. Although Dhx9 suppression sensitized both mouse and human cells to ABT-737 treatment, it did so without altering MCL-1 levels. Rather, loss of Dhx9 appeared to activate a p53-dependent apoptotic program, through aggravation of replicative stress, which was found to be both necessary and sufficient for the ABT-737-shDhx9 synthetic lethal relationship.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.