ArticleMolecular cancer2010
RHOA and PRKCZ control different aspects of cell motility in pancreatic cancer metastatic clones.
Article in Molecular cancer, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 22 citations in OpenAlex.
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- Exome Sequencing Identifies Potentially Druggable Mutations in Nasopharyngeal Carcinoma.Scientific reports · 2017Article
- Analysis of transcription profile to reveal altered signaling pathways following the overexpression of human desumoylating isopeptidase 2 in pancreatic cancer cells.Oncology letters · 2016Article
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- Atypical protein kinase C zeta: potential player in cell survival and cell migration of ovarian cancer.PloS one · 2015Article
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- Splice variant PRKC-ζ(-PrC) is a novel biomarker of human prostate cancer.British journal of cancer · 2012Article
- Interplay between FAK, PKCδ, and p190RhoGAP in the regulation of endothelial barrier function.Microvascular research · 2012Review
- Refinement of 1p36 alterations not involving PRDM16 in myeloid and lymphoid malignancies.PloS one · 2011Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundOur understanding of the mechanism regulating pancreatic cancer metastatic phenotype is limited. We analyzed the role of RHOA and PRKCZ in the motility attitude of two subclones of the pancreatic adenocarcinoma cell line SUIT-2 (S2), with different in vivo metastatic potential in nude mice: S2-m with a low metastatic potential and highly metastatic S2-CP9 using RHOA and PRKCZ cell-permeable inhibitory peptides.
methodsAdhesion assays, cell permeable peptides, RHOA activity assay, western blotting
resultsWhen used in combination cell-permeable inhibitory peptides partially inhibited cell adhesion by about 50% in clone S2-CP9. In clone S2-m, the effect was limited to 15% inhibition. In a wound healing assay, S2-CP9 was sensitive only to treatment with the combination of both RHOA and PRKCZ inhibitory peptides. Conversely, S2-m was unable to migrate toward both ends of the wound in basal conditions. Migration of cells through a membrane with 8 mum pores was completely abolished in both clones by individual treatment with RHOA and PRKCZ inhibitory peptides.
conclusionHerein, we demonstrate a critical role for RHOA and PRKCZ in the regulation of different aspects of cell motility of pancreatic adenocarcinoma and demonstrate the need to inhibit both pathways to obtain a functionally relevant effect in most assays. These results indicate that RHOA and PRKCZ, and their downstream effectors, can represent important pharmacological targets that could potentially control the highly metastatic attitude of PDAC.
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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 Socratic graph.