ArticleClinical and molecular hepatology2020
Inhibition of PI3K/Akt signaling suppresses epithelial-to-mesenchymal transition in hepatocellular carcinoma through the Snail/GSK-3/beta-catenin pathway.
Article in Clinical and molecular hepatology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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41 citing papers in PubMed, 57 citations in OpenAlex.
- Troponin: biology, molecular mechanisms, and multidimensional clinical applications.Molecular biomedicine · 2026Review
- Tectochrysin Attenuates the Chemoresistance of Hepatocellular Carcinoma Cells to Sorafenib by Inhibiting the PI3K/AKT Signaling Pathway and ABCG2 Expression.Molecular biotechnology · 2026Article
- Epithelial-Mesenchymal Transitional Markers in Endometrial Carcinoma: A Review of Clinicopathological Correlation.Cureus · 2026Review
- FAM83D facilitates EMT and metastasis of cervical cancer via interaction with GSK3β and inactivation of GSK3β/stabilization of Snail signaling.Biology direct · 2026Article
- Bicaudal‑C1 in Cancer: Molecular Mechanisms and Therapeutic Strategies Integrating Chinese and Western Medicine.Drug design, development and therapy · 2026Review
- Angelicin Inhibits NSCLC Tumor Growth via the Inhibition of Cancer-Associated Fibroblasts.Combinatorial chemistry & high throughput screening · 2026Article
- Pharmacological modulation of the PI3K/AKT/GSK3β axis: a new frontier in Alzheimer's disease treatment.Inflammopharmacology · 2026Review
- Aberrant activation of the PI3K/AKT/HIF‑1α pathway promotes glycolysis and lenvatinib resistance in liver cancer.Molecular medicine reports · 2025Article
- Targeting of the PI3 K/AKT/GSK3β Pathway in Parkinson's Disease: A Therapeutic Blueprint.Molecular neurobiology · 2025Review
- SMARCD3 Promotes Epithelial-Mesenchymal Transition in Gastric Cancer by Integrating PI3K-AKT and WNT/β-Catenin Pathways.Cancers · 2025Article
- TGFβ1-TNFα-regulated secretion of neutrophil chemokines is independent of epithelial-mesenchymal transition in breast tumor cells.Molecular biology of the cell · 2025Article
- SOAR elucidates biological insights and empowers drug discovery through spatial transcriptomics.Science advances · 2025Article
- ARID4B Promotes the Progression of Hepatocellular Carcinoma Through the PI3K/AKT Pathway.Annals of surgical oncology · 2025Article
- [C6TSEDRVAJZ, a combination of small-molecule compounds, induces differentiation of human placental fibroblasts into epithelioid cellsNan fang yi ke da xue xue bao = Journal of Southern Medical University · 2025Article
- Black rice bran‑derived anthocyanins attenuate cholangiocarcinoma cell migration via the alteration of epithelial‑mesenchymal transition and sialylation.Biomedical reports · 2025Article
- Anticancer Properties Against Select Cancer Cell Lines and Metabolomics Analysis of Tender Coconut Water.Anti-cancer agents in medicinal chemistry · 2025Article
- Knockdown of RASD1 improves MASLD progression by inhibiting the PI3K/AKT/mTOR pathway.Lipids in health and disease · 2024Article
- LINC00470 promotes malignant progression of testicular germ cell tumors.Molecular biology reports · 2024Article
- Shrimp Lipids Inhibit Migration, Epithelial-Mesenchymal Transition, and Cancer Stem Cells via Akt/mTOR/c-Myc Pathway Suppression.Biomedicines · 2024Article
- Combining lapatinib and palbociclib inhibits cell proliferation and invasion via AKT signaling pathway in endocrine-resistant breast cancer cells.Medical oncology (Northwood, London, England) · 2024Article
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8 authors at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND/
aimsPatients with advanced hepatocellular carcinoma (HCC) have a poor prognosis due to the lack of effective systemic therapies. Epithelial-to-mesenchymal transition (EMT) is a pivotal event in tumor progression, during which cancer cells acquire invasive properties. In this study, we investigated the effects of phosphatidylinositol 3-kinase (PI3K) inhibitors, including LY294002 and idelalisib, on the EMT features of HCC cells in vitro.
methodsHuman HCC cell lines, including Huh-BAT and HepG2, were used in this study. Cell proliferation was measured by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide, and cell cycle distributions were evaluated using a flow cytometer by propidium iodide staining. Immunofluorescence staining, quantitative real-time polymerase chain reaction, and immunoblotting were performed to detect EMT-associated changes.
resultsPI3K inhibitors suppressed the proliferation and invasion of HCC cells and deregulated the expression of EMT markers, as indicated by increased expression of E-cadherin, an epithelial marker, and decreased expression of N-cadherin, a mesenchymal marker, and Snail, a transcription factor implicated in EMT regulation. Furthermore, LY294002 and idelalisib inhibited the phosphorylation of GSK-3β and induced the nuclear translocation of GSK-3β, which corresponded to the downregulation of Snail and β-catenin expressions in Huh-BAT and HepG2 cells.
conclusionThe inhibition of PI3K/Akt signaling decreases Snail expression by enhancing the nuclear translocation of GSK-3β, which suppresses EMT in HCC cells, suggesting the potential clinical application of PI3K inhibitors for HCC treatment.
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