ArticleThe Journal of biological chemistry2009
Matricellular protein CCN3 (NOV) regulates actin cytoskeleton reorganization.
Article in The Journal of biological chemistry, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 37 citations in OpenAlex.
- Connexin-43 in Cancer: Above and Beyond Gap Junctions!Cancers · 2024Review
- Pleckstrin-2 Mediates the Activation of AKT in Prostate Cancer and Is Repressed by Androgen Receptor.The American journal of pathology · 2024Article
- CCN3/NOV promotes metastasis and tumor progression via GPNMB-induced EGFR activation in triple-negative breast cancer.Cell death & disease · 2023Article
- Connexins in the Heart: Regulation, Function and Involvement in Cardiac Disease.International journal of molecular sciences · 2021Review
- Connexins in Cancer: Jekyll or Hyde?Biomolecules · 2020Review
- Proteomics pinpoints alterations in grade I meningiomas of male versus female patients.Scientific reports · 2020Article
- Nov/CCN3 Enhances Cord Blood Engraftment by Rapidly Recruiting Latent Human Stem Cell Activity.Cell stem cell · 2020Article
- Gap Junctions and Wnt Signaling in the Mammary Gland: a Cross-Talk?Journal of mammary gland biology and neoplasia · 2019Review
- CCN3 promotes epithelial-mesenchymal transition in prostate cancer via FAK/Akt/HIF-1α-induced twist expression.Oncotarget · 2017Article
- CCN3-EZH2-AR feedback loop: new targets for enzalutamide and castration resistant prostate cancer.Journal of cell communication and signaling · 2017Article
- Polycomb-Mediated Disruption of an Androgen Receptor Feedback Loop Drives Castration-Resistant Prostate Cancer.Cancer research · 2017Article
- Dual roles of CCN proteins in breast cancer progression.Journal of cell communication and signaling · 2016Article
- Expression array analysis of the hepatocyte growth factor invasive program.Clinical & experimental metastasis · 2015Article
- Overexpression of connexin 43 reduces melanoma proliferative and metastatic capacity.British journal of cancer · 2015Article
- Specific Cx43 phosphorylation events regulate gap junction turnover in vivo.FEBS letters · 2014Review
- CCN3/NOV gene expression in human prostate cancer is directly suppressed by the androgen receptor.Oncogene · 2014Article
- Cx43-hemichannel function and regulation in physiology and pathophysiology: insights from the bovine corneal endothelial cell system and beyond.Frontiers in physiology · 2014Review
- hsa-mir-30c promotes the invasive phenotype of metastatic breast cancer cells by targeting NOV/CCN3.Cancer cell international · 2014Article
- Promotion of Ccn2 expression and osteoblastic differentiation by actin polymerization, which is induced by laminar fluid flow stress.Journal of cell communication and signaling · 2012Article
- CCN3 modulates bone turnover and is a novel regulator of skeletal metastasis.Journal of cell communication and signaling · 2012Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 4 countries.
Funding
Abstract
CCN3 (NOV), a putative ligand for integrin receptors, is tightly associated with the extracellular matrix and mediates diverse cellular functions, including cell adhesion and proliferation. CCN3 has been shown to negatively regulate growth although it promotes migration in a cell type-specific manner. In this study, overexpression of CCN3 reduces growth and increases intercellular adhesion of breast cancer cells. Interestingly, CCN3 overexpression also led to the formation of multiple pseudopodia that are enriched in actin, CCN3, and vinculin. Breast cancer cells preincubated with exogenous CCN3 protein also induced the same phenotype, indicating that secreted CCN3 is sufficient to induce changes in cell morphology. Surprisingly, extracellular CCN3 is internalized to the early endosomes but not to the membrane protrusions, suggesting pseudopodia-enriched CCN3 may derive from a different source. The presence of an intracellular variant of CCN3 will be consistent with our finding that the cytoplasmic tail of the gap junction protein connexin43 (Cx43) associates with CCN3. Cx43 is a channel protein permitting intercellular communication to occur. However, neither the channel properties nor the protein levels of Cx43 are affected by the CCN3 protein. In contrast, CCN3 proteins are down-regulated in the absence of Cx43. Finally, we showed that overexpression of CCN3 increases the activity of the small GTPase Rac1, thereby revealing a pathway that links Cx43 directly to actin reorganization.
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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.