ArticleOncotarget2017
Cofilin 1 induces the epithelial-mesenchymal transition of gastric cancer cells by promoting cytoskeletal rearrangement.
Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
What it found
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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
26 citing papers in PubMed, 44 citations in OpenAlex.
- Suppression of cofilin-1 promotes invasion in 3D hyaluronic acid matrices by promoting actin-based protrusions.Molecular biology of the cell · 2025Article
- Shared Biomarkers and Potential Mechanisms Between Hashimoto's Thyroiditis and Recurrent Miscarriage Revealed by Transcriptomics Analysis.International journal of general medicine · 2025Article
- Nanomechanical Characterization of Ovarian Cancer Cell Lines as a Marker of Response to 2c Treatment.International journal of molecular sciences · 2023Article
- Identification of Cofilin-1 as a novel biomarker of atopic dermatitis using iTRAQ quantitative proteomics.Journal of clinical laboratory analysis · 2022Article
- The phosphorylation level of Cofilin-1 is related to the pathological subtypes of gastric cancer.Medicine · 2022Article
- Article
- New Insights into the Roles of lncRNAs as Modulators of Cytoskeleton Architecture and Their Implications in Cellular Homeostasis and in Tumorigenesis.Non-coding RNA · 2022Review
- Epithelial plasticity in COPD results in cellular unjamming due to an increase in polymerized actin.Journal of cell science · 2022Article
- Betulonic Acid, as One of the Active Components of theMolecules (Basel, Switzerland) · 2022Article
- Oral Microbiota-Driven Cell Migration in Carcinogenesis and Metastasis.Frontiers in cellular and infection microbiology · 2022Review
- Multi-Omics Analysis of Glioblastoma and Glioblastoma Cell Line: Molecular Insights Into the Functional Role of GPR56 and TG2 in Mesenchymal Transition.Frontiers in oncology · 2022Article
- Actin Cytoskeleton and Regulation of TGFβ Signaling: Exploring Their Links.Biomolecules · 2021Review
- Unraveling the Molecular Tumor-Promoting Regulation of Cofilin-1 in Pancreatic Cancer.Cancers · 2021Article
- Cofilin-1, LIMK1 and SSH1 are differentially expressed in locally advanced colorectal cancer and according to consensus molecular subtypes.Cancer cell international · 2021Article
- The Ethyl Acetate Extract FromFrontiers in pharmacology · 2021Article
- TheFrontiers in microbiology · 2021Article
- Review
- Proteomic Investigation of Malignant Major Salivary Gland Tumors.Head and neck pathology · 2020Article
- Review
- Role of extra cellular proteins in gastric cancer progression and metastasis: an update.Genes and environment : the official journal of the Japanese Environmental Mutagen Society · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Epithelial-mesenchymal transition (EMT) is an important biological process whereby malignant tumor cells obtain the ability to migrate, invade, resist apoptosis and degrade the extracellular matrix. We found that Cofilin1 (CFL1) expression was elevated in clinical gastric cancer specimens and correlated with biomarkers of EMT in BGC-823 gastric cancer cells. BGC-823 cells exhibited EMT phenotypes and increased metastatic ability when induced by TGF-β1. By contrast, BGC-823 cells transfected with Lv-siRNA-CFL1 did not exhibit EMT phenotypes under the same inducing conditions. As CFL1 expression increased, EMT cell filopodia stretched out. In addition, the ultrastructures observed using transmission electron microscopy indicated that silencing of CFL1 markedly inhibited depolymerization of fibrous actin and cytoskeletal reorganization during EMT. Similar results were obtained in vivo. These findings demonstrate that CFL1 induces EMT by promoting cytoskeletal rearrangement. Our results may provide the basis for developing new anticancer drugs to inhibit CFL1.
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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.