ArticleCurrent research in pharmacology and drug discovery2021
Reversal of TGF-β-induced epithelial-mesenchymal transition in hepatocellular carcinoma by sorafenib, a VEGFR-2 and Raf kinase inhibitor.
Article in Current research in pharmacology and drug discovery, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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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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Who cites it
3 citing papers in PubMed, 8 citations in OpenAlex.
- Revisiting Treatment Strategies: Addressing Epithelial-to-Mesenchymal Transition-Induced Resistance in Hepatocellular Carcinoma.BME frontiers · 2025Review
- Article
- The uPA/uPAR System Orchestrates the Inflammatory Response, Vascular Homeostasis, and Immune System in Fibrosis Progression.International journal of molecular sciences · 2023Review
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
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Abstract
The epithelial-mesenchymal transition (EMT) is considered an essential process for cancer development and metastasis. Sorafenib, a RAF kinase and VEGFR-2 inhibitor, exhibits efficacy against advanced hepatocellular carcinoma (HCC), renal carcinoma, and thyroid cancer. It is well established that transforming growth factor-β (TGF-β) activated EMT is involved in the invasion and metastasis of Hep G2 cells in HCC. In this study, we investigated the effects of sorafenib on various biomarkers associated with EMT using flow cytometry. We found that sorafenib upregulated the epithelial marker E-cadherin and downregulated the mesenchymal marker vimentin. Furthermore, sorafenib downregulated the level of the EMT-inducing transcription factor SNAIL. Our findings provide insights into the mechanisms associated with the anti-EMT effects of VEGFR-2/RAF kinase inhibitors.
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