ArticleSmall GTPases2021
PKCε regulates Rho GTPases and actin cytoskeleton reorganization in non-small cell lung cancer cells.
Article in Small GTPases, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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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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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
5 citing papers in PubMed, 18 citations in OpenAlex.
- Peristalsis-Associated Mechanotransduction Drives Malignant Progression of Colorectal Cancer.Cellular and molecular bioengineering · 2023Article
- Determining KLF14 tertiary structure and diagnostic significance in brain cancer progression.Scientific reports · 2022Article
- Effect of Statins on Lung Cancer Molecular Pathways: A Possible Therapeutic Role.Pharmaceuticals (Basel, Switzerland) · 2022Review
- Activity to Breast Cancer Cell Lines of Different Malignancy and Predicted Interaction with Protein Kinase C Isoforms of Royleanones.International journal of molecular sciences · 2020Article
- Rac-GEF/Rac Signaling and Metastatic Dissemination in Lung Cancer.Frontiers in cell and developmental biology · 2020Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Oncogenic protein kinase C epsilon (PKCε) promotes the formation of membrane ruffles and motility in non-small cell lung cancer (NSCLC) cells. We found that PKCε is down-regulated when NSCLC cells undergo epithelial-to-mesenchymal transition (EMT) in response to TGF-β, thus becoming dispensable for migration and invasion in the mesenchymal state. PKCε silencing or inhibition leads to stress fibre formation, suggesting that this kinase negatively regulates RhoA activity. Ruffle formation induced by PKCε activation in the epithelial state is dependent on PI3K, but does not involve the PI3K-dependent Rac-GEFs Ect2, Trio, Vav2 or Tiam1, suggesting alternative Rac-GEFs as mediators of this response. In the proposed model, PKCε acts as a rheostat for Rho GTPases that differs in the epithelial and mesenchymal states.
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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.