ArticleCell death discovery2021
Hypoxia-induced Fascin-1 upregulation is regulated by Akt/Rac1 axis and enhances malignant properties of liver cancer cells via mediating actin cytoskeleton rearrangement and Hippo/YAP activation.
Article in Cell death discovery, 2021. 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, 19 citations in OpenAlex.
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- The impact of epithelial-mesenchymal transition (EMT) induced by metabolic processes and intracellular signaling pathways on chemo-resistance, metastasis, and recurrence in solid tumors.Cell communication and signaling : CCS · 2024Review
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- Diacylglycerol lipase alpha promotes hepatocellular carcinoma progression and induces lenvatinib resistance by enhancing YAP activity.Cell death & disease · 2023Article
- Rac1: A Regulator of Cell Migration and a Potential Target for Cancer Therapy.Molecules (Basel, Switzerland) · 2023Review
- YAP signaling is involved in WDR1-regulated proliferation and migration of non-small-cell lung cancer cells.Experimental biology and medicine (Maywood, N.J.) · 2022Article
- The role of YAP1 in liver cancer stem cells: proven and potential mechanisms.Biomarker research · 2022Review
- Expression of yes-associated protein, β-catenin and smoothened, and their clinical significance in invasive breast cancer.Experimental and therapeutic medicine · 2022Article
- Curcuminoids as Modulators of EMT in Invasive Cancers: A Review of Molecular Targets With the Contribution of Malignant Mesothelioma Studies.Frontiers in pharmacology · 2022Review
- TAZ Induces Migration of Microglia and Promotes Neurological Recovery After Spinal Cord Injury.Frontiers in pharmacology · 2022Article
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In solid tumors, hypoxia facilitates malignant progression of cancer cells by triggering epithelial-mesenchymal transition (EMT) and cancer stemness. Fascin-1, an actin-bundling protein, takes part in the formation of many actin-based cellular structures. In the present study, we explored the potential functions of hypoxia-induced upregulation of Fascin-1 in liver cancer. Transcriptome RNA-sequencing was conducted to identify hypoxia-related genes. The potential functions of Fascin-1 were evaluated by western blot, transwell migration and invasion assays, sphere-formation assay, tumor xenograft growth, gelatin zymography analysis, immunofluorescence, cell viability assay, soft agar assay, and flow cytometry. We found that Fascin-1 was upregulated by hypoxia in liver cancer cell lines, elevated in liver cancer patients and correlated with larger tumor size, lymph node metastasis, distant metastasis, and shorter overall survival. Knockdown of Fascin-1 suppressed migration, invasion, EMT, stemness, and tumor xenograft growth of liver cancer cells under both normoxia and hypoxia conditions, while forced Fascin-1 expression showed opposite effects. Moreover, hypoxia-induced upregulation of Fascin-1 was regulated by the Akt/Rac1 signaling, and inhibition of Akt/Rac1 signaling by EHop-016 and MK-2206 restrained migration, invasion, EMT, and stemness of liver cancer cells under hypoxia. Furthermore, Fascin-1 knockdown suppressed MMP-2 and MMP-9 expression, impaired actin cytoskeleton rearrangement, inactivated Hippo/YAP signaling, and increased Sorafenib sensitivity in liver cancer cells. Our study provided a novel insight of Fascin-1 in regulating migration, invasion, EMT, and stemness of liver cancer cells under normoxia and hypoxia conditions.
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Registered trials
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