ArticleCancer science2010
Myristoylated alanine-rich C kinase substrate phosphorylation promotes cholangiocarcinoma cell migration and metastasis via the protein kinase C-dependent pathway.
Article in Cancer science, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers, 1 of them a synthesis that pooled it.
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Who cites it
40 citing papers in PubMed, 1 synthesis or guideline pooled it, 63 citations in OpenAlex.
- MARCKS contributes to stromal cancer-associated fibroblast activation and facilitates ovarian cancer metastasis.Oncotarget · 2016Pooled it
- Identification of MARCKSL1 as an independent prognostic biomarker and analysis of its potential regulatory network in hepatocellular carcinoma.Discover oncology · 2026Article
- The transmembrane IL-15 isoform expressed on human melanoma cells triggers modulatory effects on tumor progression upon stimulation with the soluble IL-15Rα chain.Frontiers in immunology · 2026Article
- Integrated analysis identifies microRNA-188-5p as a suppressor of AKT/mTOR pathway in renal cancer.Cancer science · 2023Article
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- The myristoylated alanine-rich C-kinase substrates (MARCKS): A membrane-anchored mediator of the cell function.Autoimmunity reviews · 2021Review
- Pathophysiological roles of myristoylated alanine-rich C-kinase substrate (MARCKS) in hematological malignancies.Biomarker research · 2021Review
- [Affinity chromatography based phosphoproteome research on lung cancer cells and its application].Se pu = Chinese journal of chromatography · 2021Article
- Molecular targets of pomegranate (Iranian journal of basic medical sciences · 2019Review
- MARCKS and Lung Disease.American journal of respiratory cell and molecular biology · 2019Review
- MARCKS protein overexpression is associated with poor prognosis in male breast cancer.Cancer biomarkers : section A of Disease markers · 2019Article
- A Unique Family of Neuronal Signaling Proteins Implicated in Oncogenesis and Tumor Suppression.Frontiers in oncology · 2019Review
- Overexpression of MARCKS indicates a poor prognosis of oral squamous cell carcinoma.Oncology letters · 2018Article
- Stromal Expression of MARCKS Protein in Ovarian Carcinomas Has Unfavorable Prognostic Value.International journal of molecular sciences · 2017Article
- MARCKS phosphorylation is modulated by a peptide mimetic of MARCKS effector domain leading to increased radiation sensitivity in lung cancer cell lines.Oncology letters · 2017Article
- MARCKS protein overexpression in inflammatory breast cancer.Oncotarget · 2017Article
- Curcumin modulates chronic myelogenous leukemia exosomes composition and affects angiogenic phenotype via exosomal miR-21.Oncotarget · 2016Article
- Myristoylated Alanine-Rich Protein Kinase Substrate (MARCKS) Regulates Small GTPase Rac1 and Cdc42 Activity and Is a Critical Mediator of Vascular Smooth Muscle Cell Migration in Intimal Hyperplasia Formation.Journal of the American Heart Association · 2015Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Myristoylated alanine-rich C kinase substrate (MARCKS), a substrate of protein kinase C (PKC) has been suggested to be implicated in cell adhesion, secretion, and motility through the regulation of the actin cytoskeletal structure. The quantitative real-time-polymerase chain reaction analysis revealed that MARCKS is significantly overexpressed in Opisthorchis viverrini-associated cholangiocarcinoma (CCA) (P = 0.001) in a hamster model, which correlated with the results of mRNA in situ hybridization. An immunohistochemical analysis of 60 CCA patients revealed a significant increase of MARCKS expression. Moreover, the log-rank analysis indicated that CCA patients with a high MARCKS expression have significantly shorter survival times than those with a low MARCKS expression (P = 0.02). This study investigated whether MARCKS overexpression is associated with CCA metastasis. Using a confocal microscopic analysis of CCA cell lines that had been stimulated with the PKC activator, 12-0-tetradecanoyl phorbol-13-acetate (TPA), MARCKS was found to be translocated from the plasma membrane to the perinuclear area. In addition, phosphorylated MARCKS (pMARCKS) became highly concentrated in the perinuclear area. Moreover, an adhesion assay demonstrated that the exogenous overexpression of MARCKS remarkably promoted cell attachment. Interestingly, after TPA stimulation, the CCA cell line-depleted MARCKS showed a decrease in migration and invasion activity. It can be concluded that in non-stimulation, MARCKS promotes cell attachment to the extracellular matrix. After TPA stimulation, PKC phosphorylates MARCKS leading to cell migration or invasion. Taken together, the results of this study reveal a prominent role for MARCKS as one of the key players in the migration of CCA cells and suggest that cycling between MARCKS and pMARCKS can regulate the metastasis of biliary cancer cells.
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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.