ArticleMolecular oncology2012
The interaction of PKN3 with RhoC promotes malignant growth.
Article in Molecular oncology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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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.
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Who cites it
29 citing papers in PubMed, 49 citations in OpenAlex.
- Structural basis of the protein kinase PKN1 HR1 domain oligomerization and differential regulation by RhoA and Rac1.The Journal of biological chemistry · 2026Article
- Dissecting the Phospho-Regulatory Landscape of Protein Kinase N1 (PKN1) and Its Downstream Signaling: Functional Insights into the Activity-Dependent and Disease-Relevant Phosphosites.International journal of molecular sciences · 2026Article
- Small Interfering RNA Carriers for Oncotherapy: A Preclinical Overview.Pharmaceutics · 2025Review
- Small interfering RNA: From designing to therapeutic in cancer.Journal, genetic engineering & biotechnology · 2025Review
- Chemical proteomics reveals the target landscape of 1,000 kinase inhibitors.Nature chemical biology · 2024Article
- Identification of 4-Anilinoquin(az)oline as a Cell-Active Protein Kinase Novel 3 (PKN3) Inhibitor Chemotype.ChemMedChem · 2022Article
- Mechanical stress shapes the cancer cell response to neddylation inhibition.Journal of experimental & clinical cancer research : CR · 2022Article
- PRM-LIVE with Trapped Ion Mobility Spectrometry and Its Application in Selectivity Profiling of Kinase Inhibitors.Analytical chemistry · 2021Article
- The structure and function of protein kinase C-related kinases (PRKs).Biochemical Society transactions · 2021Review
- A Screen for PKN3 Substrates Reveals an Activating Phosphorylation of ARHGAP18.International journal of molecular sciences · 2020Article
- Phosphorylation Sites in Protein Kinases and Phosphatases Regulated by Formyl Peptide Receptor 2 Signaling.International journal of molecular sciences · 2020Review
- The interaction of p130Cas with PKN3 promotes malignant growth.Molecular oncology · 2019Article
- A Chemoproteomic Strategy for Direct and Proteome-Wide Covalent Inhibitor Target-Site Identification.Journal of the American Chemical Society · 2019Article
- Therapeutic effects of protein kinase N3 small interfering RNA and doxorubicin combination therapy on liver and lung metastases.Oncology letters · 2017Article
- The Race of 10 Synthetic RNAi-Based Drugs to the Pharmaceutical Market.Pharmaceutical research · 2017Review
- PKN3 is the major regulator of angiogenesis and tumor metastasis in mice.Scientific reports · 2016Article
- Recent Developments in Active Tumor Targeted Multifunctional Nanoparticles for Combination Chemotherapy in Cancer Treatment and Imaging.Journal of biomedical nanotechnology · 2015Review
- Protein kinase C-related kinase 1 and 2 play an essential role in thromboxane-mediated neoplastic responses in prostate cancer.Oncotarget · 2015Article
- RhoC Is an Unexpected Target of RhoGDI2 in Prevention of Lung Colonization of Bladder Cancer.Molecular cancer research : MCR · 2015Article
- Protein kinase N3 deficiency impedes PI3-kinase pathway-driven leukemogenesis without affecting normal hematopoiesis.Leukemia · 2015Article
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
PKN3 is an AGC-family protein kinase implicated in growth of metastatic prostate cancer cells with phosphoinositide 3-kinase pathway deregulation. The molecular mechanism, however, by which PKN3 contributes to malignant growth and tumorigenesis is not well understood. Using orthotopic mouse tumor models, we now show that inducible knockdown of PKN3 protein not only blocks metastasis, but also impairs primary prostate and breast tumor growth. Correspondingly, overexpression of exogenous PKN3 in breast cancer cells further increases their malignant behavior and invasiveness in-vitro. Mechanistically, we demonstrate that PKN3 physically interacts with Rho-family GTPases, and preferentially with RhoC, a known mediator of tumor invasion and metastasis in epithelial cancers. Likewise, RhoC predominantly associates with PKN3 compared to its closely related PKN family members. Unlike the majority of Rho GTPases and PKN molecules, which are ubiquitously expressed, both PKN3 and RhoC show limited expression in normal tissues and become upregulated in late-stage malignancies. Since PKN3 catalytic activity is increased in the presence of Rho GTPases, the co-expression and preferential interaction of PKN3 and RhoC in tumor cells are functionally relevant. Our findings provide novel insight into the regulation and function of PKN3 and suggest that the PKN3-RhoC complex represents an attractive therapeutic target in late-stage malignancies.
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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.