ArticleOncotarget2017
Systematic screening of isogenic cancer cells identifies DUSP6 as context-specific synthetic lethal target in melanoma.
Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 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.
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Who cites it
11 citing papers in PubMed, 20 citations in OpenAlex.
- DUSP6 regulates Notch1 signalling in colorectal cancer.Nature communications · 2024Article
- The cytotoxic action of BCI is not dependent on its stated DUSP1 or DUSP6 targets in neuroblastoma cells.FEBS open bio · 2022Article
- Suppression of mutant Kirsten-RAS (KRASOncogene · 2022Article
- Coordinated regulation of WNT/β-catenin, c-Met, and integrin signalling pathways by miR-193b controls triple negative breast cancer metastatic traits.BMC cancer · 2021Article
- PPP6C negatively regulates oncogenic ERK signaling through dephosphorylation of MEK.Cell reports · 2021Article
- Excess hepsin proteolytic activity limits oncogenic signaling and induces ER stress and autophagy in prostate cancer cells.Cell death & disease · 2019Article
- CFP suppresses breast cancer cell growth by TES-mediated upregulation of the transcription factor DDIT3.Oncogene · 2019Article
- Dual-specificity MAP kinase phosphatases in health and disease.Biochimica et biophysica acta. Molecular cell research · 2019Review
- Hyperactivation of ERK by multiple mechanisms is toxic to RTK-RAS mutation-driven lung adenocarcinoma cells.eLife · 2018Article
- Dual-specificity phosphatase 6 (DUSP6): a review of its molecular characteristics and clinical relevance in cancer.Cancer biology & medicine · 2018Article
- Candidate synthetic lethality partners to PARP inhibitors in the treatment of ovarian clear cell cancer.Biomedical reports · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
15 authors at 8 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Next-generation sequencing has dramatically increased genome-wide profiling options and conceptually initiates the possibility for personalized cancer therapy. State-of-the-art sequencing studies yield large candidate gene sets comprising dozens or hundreds of mutated genes. However, few technologies are available for the systematic downstream evaluation of these results to identify novel starting points of future cancer therapies.We improved and extended a site-specific recombination-based system for systematic analysis of the individual functions of a large number of candidate genes. This was facilitated by a novel system for the construction of isogenic constitutive and inducible gain- and loss-of-function cell lines. Additionally, we demonstrate the construction of isogenic cell lines with combinations of the traits for advanced functional in vitro analyses. In a proof-of-concept experiment, a library of 108 isogenic melanoma cell lines was constructed and 8 genes were identified that significantly reduced viability in a discovery screen and in an independent validation screen. Here, we demonstrate the broad applicability of this recombination-based method and we proved its potential to identify new drug targets via the identification of the tumor suppressor DUSP6 as potential synthetic lethal target in melanoma cell lines with BRAF V600E mutations and high DUSP6 expression.
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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.