ArticleOncogene2007
p120-catenin is required for the collective invasion of squamous cell carcinoma cells via a phosphorylation-independent mechanism.
Article in Oncogene, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 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
36 citing papers in PubMed, 62 citations in OpenAlex.
- Substrate heterogeneity promotes cancer cell dissemination through interface roughening.Science advances · 2026Article
- Tumour follower cells: A novel driver of leader cells in collective invasion (Review).International journal of oncology · 2023Review
- The interferon-β/STAT1 axis drives the collective invasion of skin squamous cell carcinoma with sealed intercellular spaces.Oncogenesis · 2022Article
- A requirement for p120-catenin in the metastasis of invasive ductal breast cancer.Journal of cell science · 2021Article
- p120-catenin suppresses proliferation and tumor growth of oral squamous cell carcinoma via inhibiting nuclear phospholipase C-γ1 signaling.Journal of cellular physiology · 2020Article
- PEP06 polypeptide 30 is a novel cluster-dissociating agent inhibitingActa pharmaceutica Sinica. B · 2019Article
- P120 Catenin Isoforms Differentially Associate with Breast Cancer Invasion and Metastasis.Cancers · 2019Article
- Snail-induced claudin-11 prompts collective migration for tumour progression.Nature cell biology · 2019Article
- Every step of the way: integrins in cancer progression and metastasis.Nature reviews. Cancer · 2018Review
- Loss of E-Cadherin-Dependent Cell-Cell Adhesion and the Development and Progression of Cancer.Cold Spring Harbor perspectives in biology · 2018Review
- Activation of anaphase-promoting complex by p53 induces a state of dormancy in cancer cells against chemotherapeutic stress.Oncotarget · 2016Article
- [Research progress on epithelial-mesenchymal transition in cancer recurrence and metastasis].Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2015Review
- CD151 promotes α3β1 integrin-dependent organization of carcinoma cell junctions and restrains collective cell invasion.Cancer biology & therapy · 2015Article
- PTP-PEST targets a novel tyrosine site in p120 catenin to control epithelial cell motility and Rho GTPase activity.Journal of cell science · 2014Article
- TGF-β isoforms induce EMT independent migration of ovarian cancer cells.Cancer cell international · 2014Article
- Rho GTPases in collective cell migration.Small GTPases · 2014Review
- Keratin 8 and 18 loss in epithelial cancer cells increases collective cell migration and cisplatin sensitivity through claudin1 up-regulation.The Journal of biological chemistry · 2013Article
- Concomitant loss of p120-catenin and β-catenin membrane expression and oral carcinoma progression with E-cadherin reduction.PloS one · 2013Article
- p120 catenin: an essential regulator of cadherin stability, adhesion-induced signaling, and cancer progression.Progress in molecular biology and translational science · 2013Review
- p120catenin alteration in cancer and its role in tumour invasion.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2013Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Loss of E-cadherin-mediated cell-cell junctions has been correlated with cancer cell invasion and poor patient survival. p120-catenin has emerged as a key player in promoting E-cadherin stability and adherens junction integrity and has been proposed as a potential invasion suppressor by preventing release of cells from the constraints imposed by cadherin-mediated cell-cell adhesion. However, it has been proposed that tyrosine phosphorylation of p120 may contribute to cadherin-dependent junction disassembly during invasion. Here, we use small interfering RNA (siRNA) in A431 cells to show that knockdown of p120 promotes two-dimensional migration of cells. In contrast, p120 knockdown impairs epidermal growth factor-induced A431 invasion into three-dimensional matrix gels or in organotypic culture, whereas re-expression of siRNA-resistant p120, or a p120 isoform that cannot be phosphorylated on tyrosine, restores the collective mode of invasion employed by A431 cells in vitro. Thus, p120 promotes A431 cell invasion in a phosphorylation-independent manner. We show that the collective invasion of A431 cells depends on the presence of cadherin-mediated (P- and E-cadherin) cell-cell contacts, which are lost in cells where p120 expression is knocked down. Furthermore, membranous p120 is maintained in invasive squamous cell carcinomas in tumours suggesting that p120 may be important for the collective invasion of tumours cells in vivo.
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.