ArticleCytotechnology2025
AKT activation participates in Fascin-1-induced EMT in hepatoma cells.
Article in Cytotechnology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Abstract
High expression of Fascin-1 involves high metastasis, high recurrence, and poor prognosis of cancers. However, the related regulatory mechanism in hepatocellular carcinoma (HCC) remains elusive. In this study, Fascin-1 was highly expressed in HCC tissues and cell lines. Fastin-1 protein levels and p-Akt1/Akt1 rate were increased by Akt activator SC79 and were decreased by Akt inhibitor LY294002. Silenced Fascin-1 suppressed cell proliferation, promoted cell apoptosis, suppressed cell invasion and epithelial-mesenchymal transition (EMT) in HCC cell lines. Also, silenced Fascin-1 induced cell cycle arrest in the G1 phase. Moreover, silenced Fascin-1 repressed invasion of HCC cells by inhibiting EMT. Besides, interference with Fascin-1 inhibited HCC cell growth, reduced Vimentin expressions and p-Akt1/Akt1 rate in vivo, while these impacts were abolished after injection of SC79. In conclusion, silencing Fascin-1 reduced the malignant growth of HCC, and this process was closely related to AKT inactivation. Supplementary Information: The online version contains supplementary material available at 10.1007/s10616-025-00707-9.
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