ArticleDisease models & mechanisms2013
Elevated expression of the V-ATPase C subunit triggers JNK-dependent cell invasion and overgrowth in a Drosophila epithelium.
Article in Disease models & mechanisms, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 40 citations in OpenAlex.
- RNAseK is vital for epithelial function in Drosophila melanogaster.The Journal of experimental biology · 2026Article
- TMEM184B modulates endolysosomal acidification via the vesicular proton pump.Journal of cell science · 2025Article
- The Drosophila tumour suppressor Lgl and Vap33 activate the Hippo pathway through a dual mechanism.Journal of cell science · 2024Article
- The transcription factor Spalt and human homologue SALL4 induce cell invasion via the dMyc-JNK pathway inBiology open · 2020Article
- Investigation of Isoform Specific Functions of the V-ATPase a Subunit DuringFrontiers in genetics · 2020Article
- Two-Faced: Roles of JNK Signalling During Tumourigenesis in theFrontiers in cell and developmental biology · 2020Review
- C1 Silencing Attenuates Inflammation and Alveolar Bone Resorption in Endodontic Disease.Journal of endodontics · 2019Article
- Genetic and Cell Biology Methods to Study ESCRTs in Drosophila melanogaster.Methods in molecular biology (Clifton, N.J.) · 2019Article
- Time-resolved transcriptomics in neural stem cells identifies a v-ATPase/Notch regulatory loop.The Journal of cell biology · 2018Article
- Lgl reduces endosomal vesicle acidification and Notch signaling by promoting the interaction between Vap33 and the V-ATPase complex.Science signaling · 2018Article
- Modelling Cooperative Tumorigenesis inBioMed research international · 2018Review
- Tumour acidosis: from the passenger to the driver's seat.Nature reviews. Cancer · 2017Review
- Cancer cell behaviors mediated by dysregulated pH dynamics at a glance.Journal of cell science · 2017Review
- The Function of V-ATPases in Cancer.Physiological reviews · 2016Review
- The Drosophila tricellular junction protein Gliotactin regulates its own mRNA levels through BMP-mediated induction of miR-184.Journal of cell science · 2016Article
- Control of lysosomal biogenesis and Notch-dependent tissue patterning by components of the TFEB-V-ATPase axis in Drosophila melanogaster.Autophagy · 2016Article
- Expression and role of V1A subunit of V-ATPases in gastric cancer cells.International journal of clinical oncology · 2015Article
- Article
- Increased H⁺ efflux is sufficient to induce dysplasia and necessary for viability with oncogene expression.eLife · 2015Article
- Regulation of Notch signaling and endocytosis by the Lgl neoplastic tumor suppressor.Cell cycle (Georgetown, Tex.) · 2015Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The C subunit of the vacuolar H(+)-ATPase or V-ATPase regulates the activity and assembly of the proton pump at cellular membranes. It has been shown to be strongly upregulated in oral squamous cell carcinoma, a highly metastatic epithelial cancer. In addition, increased V-ATPase activity appears to correlate with invasiveness of cancer cells, but the underlying mechanism is largely unknown. Using the Drosophila wing imaginal epithelium as an in vivo model system, we demonstrate that overexpression of Vha44, the Drosophila orthologue of the C subunit, causes a tumor-like tissue transformation in cells of the wing epithelium. Overexpressing cells are excluded from the epithelium and acquire invasive properties while displaying high apoptotic rates. Blocking apoptosis in these cells unmasks a strong proliferation stimulus, leading to overgrowth. Furthermore, we show that excess Vha44 greatly increases acidification of endocytic compartments and interferes with endosomal trafficking. As a result, cargoes such as GFP-Lamp1 and Notch accumulate in highly acidified enlarged endolysosomal compartments. Consistent with previous reports on the endocytic activation of Eiger/JNK signaling, we find that V-ATPase stimulation by Vha44 causes JNK signaling activation whereas downmodulation of JNK signaling rescues the invasive phenotypes. In summary, our in vivo-findings demonstrate that increased levels of V-ATPase C subunit induce a Eiger/JNK-dependent cell transformation within an epithelial organ that recapitulates early carcinoma stages.
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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.