ArticleAmerican journal of translational research2019
Apogossypolone acts as a metastasis inhibitor via up-regulation of E-cadherin dependent on the GSK-3/AKT complex.
Article in American journal of translational research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
4 citing papers in PubMed.
- Apogossypolone Inhibits Cell Proliferation and Epithelial-Mesenchymal Transition in Cervical CancerFrontiers in oncology · 2022Article
- Oridonin inhibits the migration and epithelial-to-mesenchymal transition of small cell lung cancer cells by suppressing FAK-ERK1/2 signalling pathway.Journal of cellular and molecular medicine · 2020Article
- Uncoupling Traditional Functionalities of Metastasis: The Parting of Ways with Real-Time Assays.Journal of clinical medicine · 2019Review
- The Identification of Differentially Expressed Genes Showing Aberrant Methylation Patterns in Pheochromocytoma by Integrated Bioinformatics Analysis.Frontiers in genetics · 2019Article
Corrections and comments
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Authors and funding
11 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Malignant pheochromocytoma is exactly diagnosed only upon the occurrence of metastatic foci. At that point, however, patients are less likely to experience many benefits from traditional chemotherapy. Therefore, a strategy worthy of consideration is inhibition or delay of metastasis with drugs. Recently, numerous studies have indicated that epithelial-to-mesenchymal transition (EMT) is involved in malignant pheochromocytoma, where there is over-expression of metastatic promoting genes and low expression of metastatic suppressor genes. In previous research, we confirmed that apogossypolone (ApoG2) could effectively inhibit tumor movement capabilities, but potential mechanisms for the inhibition were unknown. Here, we initially corroborated that ApoG2 could induce GSK-3/AKT complex formation to down-regulate phosphorylation of the PI3K/AKT pathway. Subsequently, ApoG2 inhibited cell mobilities via promotion of E-cadherin and β-catenin translocation from cytoplasm to membrane dependent on down-regulate of the PI3K/AKT pathway. Unexpectedly, ApoG2 seemed to promote tumor progression, instead of suppression when there were circulating tumor cells
Indexed as
Identifiers
30787981PMC6357321What OpenQuestion holds
Registered trials
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