ArticleThe Journal of clinical investigation2017
p120-Catenin is an obligate haploinsufficient tumor suppressor in intestinal neoplasia.
Article in The Journal of clinical investigation, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 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
16 citing papers in PubMed, 31 citations in OpenAlex.
- Kaiso mediates transcription and RNA splicing in colorectal carcinoma: role of BRCA1 in the Kaiso enhanceosome.Open biology · 2025Article
- Enhancement of Autophagy in Macrophages via the p120-Catenin-Mediated mTOR Signaling Pathway.Journal of immunology (Baltimore, Md. : 1950) · 2024Article
- Genomic and epigenomic basis of breast invasive lobular carcinomas lacking CDH1 genetic alterations.NPJ precision oncology · 2024Article
- Oridonin promotes endoplasmic reticulum stress via TP53-repressed TCF4 transactivation in colorectal cancer.Journal of experimental & clinical cancer research : CR · 2023Article
- Cadherins and catenins in cancer: connecting cancer pathways and tumor microenvironment.Frontiers in cell and developmental biology · 2023Review
- MTG16 regulates colonic epithelial differentiation, colitis, and tumorigenesis by repressing E protein transcription factors.JCI insight · 2022Article
- KRAS phosphorylation regulates cell polarization and tumorigenic properties in colorectal cancer.Oncogene · 2021Article
- A requirement for p120-catenin in the metastasis of invasive ductal breast cancer.Journal of cell science · 2021Article
- EpCAM is essential for maintenance of the small intestinal epithelium architecture via regulation of the expression and localization of proteins that compose adherens junctions.International journal of molecular medicine · 2021Article
- p120-catenin phosphorylation status alters E-cadherin mediated cell adhesion and ability of tumor cells to metastasize.PloS one · 2020Article
- Role of α-Catenin and its mechanosensing properties in regulating Hippo/YAP-dependent tissue growth.PLoS genetics · 2019Article
- P120 Catenin Isoforms Differentially Associate with Breast Cancer Invasion and Metastasis.Cancers · 2019Article
- Rho kinase-dependent apical constriction counteracts M-phase apical expansion to enable mouse neural tube closure.Journal of cell science · 2019Article
- E-cadherin Beyond Structure: A Signaling Hub in Colon Homeostasis and Disease.International journal of molecular sciences · 2019Review
- Regulation of Epithelial Plasticity Determines Metastatic Organotropism in Pancreatic Cancer.Developmental cell · 2018Article
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors at 4 institutions in 4 countries.
Funding
Abstract
p120-Catenin (p120) functions as a tumor suppressor in intestinal cancer, but the mechanism is unclear. Here, using conditional p120 knockout in Apc-sensitized mouse models of intestinal cancer, we have identified p120 as an "obligatory" haploinsufficient tumor suppressor. Whereas monoallelic loss of p120 was associated with a significant increase in tumor multiplicity, loss of both alleles was never observed in tumors from these mice. Moreover, forced ablation of the second allele did not further enhance tumorigenesis, but instead induced synthetic lethality in combination with Apc loss of heterozygosity. In tumor-derived organoid cultures, elimination of both p120 alleles resulted in caspase-3-dependent apoptosis that was blocked by inhibition of Rho kinase (ROCK). With ROCK inhibition, however, p120-ablated organoids exhibited a branching phenotype and a substantial increase in cell proliferation. Access to data from Sleeping Beauty mutagenesis screens afforded an opportunity to directly assess the tumorigenic impact of p120 haploinsufficiency relative to other candidate drivers. Remarkably, p120 ranked third among the 919 drivers identified. Cofactors α-catenin and epithelial cadherin (E-cadherin) were also among the highest scoring candidates, indicating a mechanism at the level of the intact complex that may play an important role at very early stages of of intestinal tumorigenesis while simultaneously restricting outright loss via synthetic lethality.
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.