ArticleeLife2016
In vivo genetic dissection of tumor growth and the Warburg effect.
Article in eLife, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
60 citing papers in PubMed, 102 citations in OpenAlex.
- Article
- HIF-1α-mediated feedback prevents TOR signalling from depleting oxygen supply and triggering stress during normal development.Nature communications · 2025Article
- Activation of a Src-JNK pathway in unscheduled endocycling cells of the Drosophila wing disc induces a chronic wounding response.Genetics · 2025Article
- Mitochondrial ROS and HIF-1α signaling mediate synaptic plasticity in the critical period.PLoS biology · 2025Article
- Intratumor HIF-1α modulates production of a cachectic ligand to cause host wasting.Cell insight · 2025Article
- Epigenetic reprogramming induced by key metabolite depletion is an evolutionarily ancient path to tumorigenesis.Disease models & mechanisms · 2025Article
- Hypoxia-inducible factor 1α is required to establish the larval glycolytic program in Drosophila melanogaster.Molecular metabolism · 2025Article
- Hypoxia-inducible factor 1α is required to establish the larval glycolytic program inbioRxiv : the preprint server for biology · 2025Article
- Nonautonomous Regulation of Tumor Growth.Advances in experimental medicine and biology · 2025Review
- Review
- Article
- Metabolic Recoding of NSUN2-Mediated mAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Article
- A conserved mechanism for JNK-mediated loss of Notch function in advanced prostate cancer.Science signaling · 2023Article
- Characterization of genetic and molecular tools for studying the endogenous expression ofbioRxiv : the preprint server for biology · 2023Article
- Immunometabolic regulation during the presence of microorganisms and parasitoids in insects.Frontiers in immunology · 2023Review
- TG2 as a novel breast cancer prognostic marker promotes cell proliferation and glycolysis by activating the MEK/ERK/LDH pathway.BMC cancer · 2022Article
- Tumor elimination by clustered microRNAs miR-306 and miR-79 via noncanonical activation of JNK signaling.eLife · 2022Article
- Blood progenitor redox homeostasis through olfaction-derived systemic GABA in hematopoietic growth control in Drosophila.Development (Cambridge, England) · 2022Article
- Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
A well-characterized metabolic landmark for aggressive cancers is the reprogramming from oxidative phosphorylation to aerobic glycolysis, referred to as the Warburg effect. Models mimicking this process are often incomplete due to genetic complexities of tumors and cell lines containing unmapped collaborating mutations. In order to establish a system where individual components of oncogenic signals and metabolic pathways can be readily elucidated, we induced a glycolytic tumor in the Drosophila wing imaginal disc by activating the oncogene PDGF/VEGF-receptor (Pvr). This causes activation of multiple oncogenic pathways including Ras, PI3K/Akt, Raf/ERK, Src and JNK. Together this network of genes stabilizes Hifα (Sima) that in turn, transcriptionally up-regulates many genes encoding glycolytic enzymes. Collectively, this network of genes also causes inhibition of pyruvate dehydrogenase (PDH) activity resulting in diminished ox-phos levels. The high ROS produced during this process functions as a feedback signal to consolidate this metabolic reprogramming.
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.