ArticleOncotarget2016
Gelsolin-mediated activation of PI3K/Akt pathway is crucial for hepatocyte growth factor-induced cell scattering in gastric carcinoma.
Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 18 citations in OpenAlex.
- Iron-responsive ZNF185 overexpression drives mitochondrial fission and endoplasmic reticulum stress via cytoskeletal remodeling in granulosa cells.Cell death discovery · 2025Article
- Phenotypic rescue via mTOR inhibition in neuron-specific Pten knockout mice reveals AKT and mTORC1-site specific changes.Molecular psychiatry · 2025Article
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- A simplified in vitro disease-mimicking culture system can determine the angiogenic effect of medicines on vascular diseases.Cytotechnology · 2025Article
- Actin polymerization and depolymerization in developing vertebrates.Frontiers in physiology · 2023Review
- Review
- Susceptibility of cytoskeletal-associated proteins for tumor progression.Cellular and molecular life sciences : CMLS · 2021Review
- Morphological features of single cells enable accurate automated classification of cancer from non-cancer cell lines.Scientific reports · 2021Article
- Review
- Inhibition of TDP43-Mediated SNHG12-miR-195-SOX5 Feedback Loop Impeded Malignant Biological Behaviors of Glioma Cells.Molecular therapy. Nucleic acids · 2018Article
- Gelsolin regulates proliferation, apoptosis and invasion in natural killer/T-cell lymphoma cells.Biology open · 2018Article
- Article
- Does urinary peptide content differ between COPD patients with and without inherited alpha-1 antitrypsin deficiency?International journal of chronic obstructive pulmonary disease · 2017Article
Corrections and comments
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Authors and funding
24 authors at 9 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In gastric cancer (GC), the main subtypes (diffuse and intestinal types) differ in pathological characteristics, with diffuse GC exhibiting early disseminative and invasive behaviour. A distinctive feature of diffuse GC is loss of intercellular adhesion. Although widely attributed to mutations in the CDH1 gene encoding E-cadherin, a significant percentage of diffuse GC do not harbor CDH1 mutations. We found that the expression of the actin-modulating cytoskeletal protein, gelsolin, is significantly higher in diffuse-type compared to intestinal-type GCs, using immunohistochemical and microarray analysis. Furthermore, in GCs with wild-type CDH1, gelsolin expression correlated inversely with CDH1 gene expression. Downregulating gelsolin using siRNA in GC cells enhanced intercellular adhesion and E-cadherin expression, and reduced invasive capacity. Interestingly, hepatocyte growth factor (HGF) induced increased gelsolin expression, and gelsolin was essential for HGF-medicated cell scattering and E-cadherin transcriptional repression through Snail, Twist and Zeb2. The HGF-dependent effect on E-cadherin was found to be mediated by interactions between gelsolin and PI3K-Akt signaling. This study reveals for the first time a function of gelsolin in the HGF/cMet oncogenic pathway, which leads to E-cadherin repression and cell scattering in gastric cancer. Our study highlights gelsolin as an important pro-disseminative factor contributing to the aggressive phenotype of diffuse GC.
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