ArticleMolecular oncology2019
The interaction of p130Cas with PKN3 promotes malignant growth.
Article in Molecular oncology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 18 citations in OpenAlex.
- Differential response of MDA‑MB‑231 breast cancer and MCF10A normal breast cells to cytoskeletal disruption.Oncology reports · 2023Article
- KSFinder-a knowledge graph model for link prediction of novel phosphorylated substrates of kinases.PeerJ · 2023Article
- Identification of 4-Anilinoquin(az)oline as a Cell-Active Protein Kinase Novel 3 (PKN3) Inhibitor Chemotype.ChemMedChem · 2022Article
- Article
- Mechanical stress shapes the cancer cell response to neddylation inhibition.Journal of experimental & clinical cancer research : CR · 2022Article
- The structure and function of protein kinase C-related kinases (PRKs).Biochemical Society transactions · 2021Review
- Protumor Effects of Histone H3-H4 Chaperone Antisilencing Feature 1B Gene on Lung Adenocarcinoma: In Silico andComputational and mathematical methods in medicine · 2021Article
- Integrated Analysis of ceRNA Network Reveals Prognostic and Metastasis Associated Biomarkers in Breast Cancer.Frontiers in oncology · 2021Article
- BCAR1 promotes proliferation and cell growth in lung adenocarcinoma via upregulation of POLR2A.Thoracic cancer · 2020Article
- A Screen for PKN3 Substrates Reveals an Activating Phosphorylation of ARHGAP18.International journal of molecular sciences · 2020Article
- CSRP2 suppresses colorectal cancer progressionTheranostics · 2020Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Protein p130Cas constitutes an adaptor protein mainly involved in integrin signaling downstream of Src kinase. Owing to its modular structure, p130Cas acts as a general regulator of cancer cell growth and invasiveness induced by different oncogenes. However, other mechanisms of p130Cas signaling leading to malignant progression are poorly understood. Here, we show a novel interaction of p130Cas with Ser/Thr kinase PKN3, which is implicated in prostate and breast cancer growth downstream of phosphoinositide 3-kinase. This direct interaction is mediated by the p130Cas SH3 domain and the centrally located PKN3 polyproline sequence. PKN3 is the first identified Ser/Thr kinase to bind and phosphorylate p130Cas and to colocalize with p130Cas in cell structures that have a pro-invasive function. Moreover, the PKN3-p130Cas interaction is important for mouse embryonic fibroblast growth and invasiveness independent of Src transformation, indicating a mechanism distinct from that previously characterized for p130Cas. Together, our results suggest that the PKN3-p130Cas complex represents an attractive therapeutic target in late-stage malignancies.
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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.