ArticleCancer gene therapy2014
Akt-mediated transforming growth factor-β1-induced epithelial-mesenchymal transition in cultured human esophageal squamous cancer cells.
Article in Cancer gene therapy, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 10 citations in OpenAlex.
- Potential markers of cancer stem-like cells in ESCC: a review of the current knowledge.Frontiers in oncology · 2023Review
- Transient Receptor Potential Channel 6 Knockout Ameliorates Kidney Fibrosis by Inhibition of Epithelial-Mesenchymal Transition.Frontiers in cell and developmental biology · 2020Article
- Human papillomavirus type 18 oncoproteins exert their oncogenicity in esophageal and tongue squamous cell carcinoma cell lines distinctly.BMC cancer · 2019Article
- Role of matrix metalloproteinase-9 in transforming growth factor-β1-induced epithelial-mesenchymal transition in esophageal squamous cell carcinoma.OncoTargets and therapy · 2017Article
- Article
- Sonic hedgehog-Gli1 signals promote epithelial-mesenchymal transition in ovarian cancer by mediating PI3K/AKT pathway.Medical oncology (Northwood, London, England) · 2015Article
- CSN5 silencing inhibits invasion and arrests cell cycle progression in human colorectal cancer SW480 and LS174T cells in vitro.International journal of clinical and experimental pathology · 2015Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Epithelial-mesenchymal transition (EMT) has a crucial role during embryonic development and has also come under intense scrutiny as a mechanism through which esophageal squamous cell cancer (ESCC) progresses to become metastatic. Transforming growth factor beta (TGF-β)-mediated EMT has been observed in a variety of cell types and has been identified as the main inducer of EMT in many types of cancer. Akt activity is involved in TGF-β-mediated EMT; however, its precise relationship and role in EMT in ESCC has not been well explained to date. Our data demonstrated that in human ESCC tissues Akt and its activated form, phosphorylated-Akt (p-Akt), were overexpressed; in addition, Akt and p-Akt were negatively correlated with epithelial cadherin (E-cadherin). In EC-9706 cells, exogenous TGF-β1 could induce EMT and at the same time could increase the EC-9706 cell invasive and metastatic ability. Moreover, Akt knockdown by small-interfering RNA could attenuate the EMT induced by TGF-β1 by increasing the epithelial marker E-cadherin and decreasing the mesenchymal marker Vimentin. Silencing Akt expression could decrease the migration ability of EC-9706 cells efficiently. In short, Akt is likely to have a more important role in the EMT induced by TGF-β1 in EC-9706 and may contribute to the invasive and metastatic ability of EC-9706. Akt may be an effective therapeutic in advanced and metastatic ESCC.
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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.