ArticleNature communications2014
The tumour suppressor DLC2 ensures mitotic fidelity by coordinating spindle positioning and cell-cell adhesion.
Article in Nature communications, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
What it found
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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.
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Who cites it
11 citing papers in PubMed, 24 citations in OpenAlex.
- Oncogenic Ras deregulates cell-substrate interactions during mitotic rounding and respreading to alter cell division orientation.Current biology : CB · 2023Article
- StarD13: a potential star target for tumor therapeutics.Human cell · 2020Review
- Differential Allele-Specific Expression Uncovers Breast Cancer Genes Dysregulated by Cis Noncoding Mutations.Cell systems · 2020Article
- High expression of DLC family proteins predicts better prognosis and inhibits tumor progression in NSCLC.Molecular medicine reports · 2019Article
- Mechanism of cell-intrinsic adaptation to Adams-Oliver Syndrome gene DOCK6 disruption highlights ubiquitin-like modifier ISG15 as a regulator of RHO GTPases.Small GTPases · 2019Article
- DLC2 operates as a tumor suppressor gene in breast cancer via the RhoGTPase pathway.Oncology letters · 2019Article
- Signaling by Small GTPases at Cell-Cell Junctions: Protein Interactions Building Control and Networks.Cold Spring Harbor perspectives in biology · 2018Review
- DLC2 inhibits development of glioma through regulating the expression ratio of TAp73α/TAp73β.American journal of cancer research · 2018Article
- Downregulation of STARD8 in gastric cancer and its involvement in gastric cancer progression.OncoTargets and therapy · 2018Article
- Deregulation of Rho GTPases in cancer.Small GTPases · 2016Review
- Effects of various stages of nephropathy on wound healing in patients with diabetes: an observational cohort study encompassing 731 diabetics.International urology and nephrology · 2016Observational
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
Dividing epithelial cells need to coordinate spindle positioning with shape changes to maintain cell-cell adhesion. Microtubule interactions with the cell cortex regulate mitotic spindle positioning within the plane of division. How the spindle crosstalks with the actin cytoskeleton to ensure faithful mitosis and spindle positioning is unclear. Here we demonstrate that the tumour suppressor DLC2, a negative regulator of Cdc42, and the interacting kinesin Kif1B coordinate cell junction maintenance and planar spindle positioning by regulating microtubule growth and crosstalk with the actin cytoskeleton. Loss of DLC2 induces the mislocalization of Kif1B, increased Cdc42 activity and cortical recruitment of the Cdc42 effector mDia3, a microtubule stabilizer and promoter of actin dynamics. Accordingly, DLC2 or Kif1B depletion promotes microtubule stabilization, defective spindle positioning, chromosome misalignment and aneuploidy. The tumour suppressor DLC2 and Kif1B are thus central components of a signalling network that guides spindle positioning, cell-cell adhesion and mitotic fidelity.
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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.