ArticleiScience2020
ZAK Inhibitor PLX4720 Promotes Extrusion of Transformed Cells via Cell Competition.
Article in iScience, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 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
7 citing papers in PubMed, 11 citations in OpenAlex.
- ZAK kinase at the crossroads of cellular stress: functional plasticity, human pathobiology, and precision therapeutics.Frontiers in cell and developmental biology · 2026Review
- LncRNA LINC02381/miR-133b axis promotes tumorigenesis and predicts survival in pancreatic cancer.Discover oncology · 2025Article
- Myofibrillar myopathy hallmarks associated with ZAK deficiency.Human molecular genetics · 2023Article
- Pleiotropic effects of cell competition between normal and transformed cells in mammalian cancers.Journal of cancer research and clinical oncology · 2023Review
- Activation of the NLRP1 inflammasome in human keratinocytes by the dsDNA mimetic poly(dA:dT).Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Epithelial cells remove precancerous cells by cell competition via MHC class I-LILRB3 interaction.Nature immunology · 2021Article
- Early mechanical selection of cell extrusion and extrusion signaling in cancer.Current opinion in cell biology · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Previous studies have revealed that, at the initial step of carcinogenesis, transformed cells are often eliminated from epithelia via cell competition with the surrounding normal cells. In this study, we performed cell competition-based high-throughput screening for chemical compounds using cultured epithelial cells and confocal microscopy. PLX4720 was identified as a hit compound that promoted apical extrusion of RasV12-transformed cells surrounded by normal epithelial cells. Knockdown/knockout of ZAK, a target of PLX4720, substantially enhanced the apical elimination of RasV12 cells in vitro and in vivo. ZAK negatively modulated the accumulation or activation of multiple cell competition regulators. Moreover, PLX4720 treatment promoted apical elimination of RasV12-transformed cells in vivo and suppressed the formation of potentially precancerous tumors. This is the first report demonstrating that a cell competition-promoting chemical drug facilitates apical elimination of transformed cells in vivo, providing a new dimension in cancer preventive medicine.
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.