ArticleThe Journal of cell biology2018
Loss of E-cadherin provides tolerance to centrosome amplification in epithelial cancer cells.
Article in The Journal of cell biology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 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
47 citing papers in PubMed, 78 citations in OpenAlex.
- CenSegNet: a generalist high-throughput deep learning framework for centrosome phenotyping at spatial and single-cell resolution in heterogeneous tissues.Nature communications · 2026Article
- Sensing centrosome amplification: the interface between centriole duplication and autophagy.Nature communications · 2026Article
- The PLK4 inhibitor RP-1664 demonstrates potent efficacy in neuroblastoma preclinical models through a dual mechanism of sensitivity.Nature communications · 2026Article
- Matrix Mechanics Governs Mechano-Metabolic Adaptation across Cancer Grades in Bladder Spheroids.ACS applied materials & interfaces · 2026Article
- KIFC1 is Associated With Sarcomatoid Differentiation, Immune Response, and a Poor Prognosis in Clear Cell Renal Cell Carcinoma.Cancer medicine · 2026Article
- Synaptic vesicle glycoprotein 2 enables viable aneuploidy following centrosome amplification.Genetics · 2025Article
- The Kinesin-14 tail: Dual microtubule binding domains drive spindle morphogenesis through tight microtubule cross-linking and robust sliding.Molecular biology of the cell · 2025Article
- Force transmission is a master regulator of mechanical cell competition.Nature materials · 2025Article
- Surviving the Storm: The Role of Poly- and Depolyploidization in Tissues and Tumors.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Review
- Mechanical stress combines with planar polarised patterning during metaphase to orient embryonic epithelial cell divisions.Development (Cambridge, England) · 2024Article
- Interplay between the plasma membrane and cell-cell adhesion maintains epithelial identity for correct polarised cell divisions.Journal of cell science · 2024Article
- Inhibiting centrosome clustering reduces cystogenesis and improves kidney function in autosomal dominant polycystic kidney disease.JCI insight · 2024Article
- Cortical dynein drives centrosome clustering in cells with centrosome amplification.Molecular biology of the cell · 2023Article
- Whole-Genome Duplication and Genome Instability in Cancer Cells: Double the Trouble.International journal of molecular sciences · 2023Review
- Epigenetic alterations impede epithelial-mesenchymal transition by modulating centrosome amplification and Myc/RAS axis in triple negative breast cancer cells.Scientific reports · 2023Article
- Terminally differentiated osteoclasts organize centrosomes into large clusters for microtubule nucleation and bone resorption.Molecular biology of the cell · 2022Article
- Targeting genome integrity dysfunctions impedes metastatic potency in non-small cell lung cancer circulating tumor cell-derived explants.JCI insight · 2022Article
- Keep Calm and Carry on with Extra Centrosomes.Cancers · 2022Review
- Kinesin Family Member C1 (KIFC1/HSET): A Potential Actionable Biomarker of Early Stage Breast Tumorigenesis and Progression of High-Risk Lesions.Journal of personalized medicine · 2021Review
- Modeling reveals cortical dynein-dependent fluctuations in bipolar spindle length.Biophysical journal · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 5 institutions in 1 country.
Funding
Abstract
Centrosome amplification is a common feature of human tumors. To survive, cancer cells cluster extra centrosomes during mitosis, avoiding the detrimental effects of multipolar divisions. However, it is unclear whether clustering requires adaptation or is inherent to all cells. Here, we show that cells have varied abilities to cluster extra centrosomes. Epithelial cells are innately inefficient at clustering even in the presence of HSET/KIFC1, which is essential but not sufficient to promote clustering. The presence of E-cadherin decreases cortical contractility during mitosis through a signaling cascade leading to multipolar divisions, and its knockout promotes clustering and survival of cells with multiple centrosomes. Cortical contractility restricts centrosome movement at a minimal distance required for HSET/KIFC1 to exert its function, highlighting a biphasic model for centrosome clustering. In breast cancer cell lines, increased levels of centrosome amplification are accompanied by efficient clustering and loss of E-cadherin, indicating that this is an important adaptation mechanism to centrosome amplification in cancer.
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.