ArticleCancer research2011
DLC1 interaction with S100A10 mediates inhibition of in vitro cell invasion and tumorigenicity of lung cancer cells through a RhoGAP-independent mechanism.
Article in Cancer research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
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Who cites it
43 citing papers in PubMed, 60 citations in OpenAlex.
- Crosstalk Between CTSBAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- A review on clinical implications of S100 proteins in lung diseases.Frontiers in medicine · 2025Review
- Exploitation of the fibrinolytic system by B-cell acute lymphoblastic leukemia and its therapeutic targeting.Nature communications · 2024Article
- S100A10 promotes cancer metastasis via recruitment of MDSCs within the lungs.Oncoimmunology · 2024Article
- Recent Advances in Molecular and Cellular Functions of S100A10.Biomolecules · 2023Review
- S100 calcium-binding protein A10 contributes to malignant traits in osteosarcoma cells by regulating glycolytic metabolism via the AKT/mTOR pathway.Bioengineered · 2022Article
- ARHGAP24 represses β-catenin transactivation-induced invasiveness in hepatocellular carcinoma mainly by acting as a GTPase-independent scaffold.Theranostics · 2022Article
- The Annexin A2/S100A10 Complex: The Mutualistic Symbiosis of Two Distinct Proteins.Biomolecules · 2021Review
- The ANXA2/S100A10 Complex-Regulation of the Oncogenic Plasminogen Receptor.Biomolecules · 2021Review
- S100 Calcium Binding Protein A10, A Novel Oncogene, Promotes the Proliferation, Invasion, and Migration of Hepatocellular Carcinoma.Frontiers in genetics · 2021Article
- DLC1 SAM domain-binding peptides inhibit cancer cell growth and migration by inactivating RhoA.The Journal of biological chemistry · 2020Article
- Predictions of the dysregulated competing endogenous RNA signature involved in the progression of human lung adenocarcinoma.Cancer biomarkers : section A of Disease markers · 2020Article
- Identification and Analysis of Dysfunctional Genes and Pathways in CD8Frontiers in genetics · 2020Article
- Critical role and its underlying molecular events of the plasminogen receptor, S100A10 in malignant tumor and non-tumor diseases.Journal of Cancer · 2020Review
- S100A10 silencing suppresses proliferation, migration and invasion of ovarian cancer cells and enhances sensitivity to carboplatin.Journal of ovarian research · 2019Article
- High expression of DLC family proteins predicts better prognosis and inhibits tumor progression in NSCLC.Molecular medicine reports · 2019Article
- The prognostic value of S100A10 expression in cancer.Oncology letters · 2019Review
- CPT1A-mediated succinylation of S100A10 increases human gastric cancer invasion.Journal of cellular and molecular medicine · 2019Article
- P11 Loss-of-Function is Associated with Decreased Cell Proliferation and Neurobehavioral Disorders in Mice.International journal of biological sciences · 2019Article
- S100A10 and Cancer Hallmarks: Structure, Functions, and its Emerging Role in Ovarian Cancer.International journal of molecular sciences · 2018Review
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
The DLC1 gene encodes a Rho GTPase-activating protein (RhoGAP) that functions as a tumor suppressor in several common human cancers. The multidomain structure of DLC1 enables interaction with a number of other proteins. Here we report that the proinflammatory protein S100A10 (also known as p11), a key cell surface receptor for plasminogen which regulates pericellular proteolysis and tumor cell invasion, is a new binding partner of DLC1 in human cells. We determined that the 2 proteins colocalize in the cell cytoplasm and that their binding is mediated by central sequences in the central domain of DLC1 and the C-terminus of S100A10. Because the same S100A10 sequence also mediates binding to Annexin 2, we found that DLC1 competed with Annexin 2 for interaction with S100A10. DLC1 binding to S100A10 did not affect DLC1's RhoGAP activity, but it decreased the steady-state level of S100A10 expression in a dose-dependent manner by displacing it from Annexin 2 and making it accessible to ubiquitin-dependent degradation. This process attenuated plasminogen activation and resulted in inhibition of in vitro cell migration, invasion, colony formation, and anchorage-independent growth of aggressive lung cancer cells. These results suggest that a novel GAP-independent mechanism contributes to the tumor suppressive activity of DLC1, and highlight the importance and complexity of protein-protein interactions involving DLC1 in certain cancers.
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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.