ArticleAmerican journal of translational research2019
Blocking transforming growth factor-beta reduces the migration and invasion of the residual tumour after TAE.
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, 5 citations in OpenAlex.
- Review
- Diverse Neutrophil Functions in Cancer and Promising Neutrophil-Based Cancer Therapies.International journal of molecular sciences · 2022Review
- Review
- Modulation of the TGF-β signaling pathway by long noncoding RNA in hepatocellular carcinoma.Biomarker research · 2020Review
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
This study aimed to investigate the treatment effects of combining TAE therapy with LY2109761, a transforming growth factor-beta (TGF-β) receptor I kinase inhibitor, on suppressing tumour growth and metastasis. We simulated the changing tumour microenvironment before and after TAE using both in vitro and in vivo models. In vitro, we evaluated the altered migration and invasion properties of HepG2 cells using migration and invasion assays. In addition, western blot analysis was used to investigate molecular mechanisms underlying the biological activities of LY2109761 in HepG2 cells. In vivo, we combined LY2109761 with TAE together in the VX2 rabbit model to evaluate the therapeutic effects of the combination. In vitro, the Smad pathway were substantially activated by hypoxia, and LY2109761 significantly inhibited the Smad pathway under both normoxic and hypoxic circumstances. Furthermore, LY2109761 inhibited cell proliferation, intravasation and metastasis by downregulating Smad-2 phosphorylation and up-regulating E-cadherin expression in both normoxic and hypoxic conditions. In addition, in animals, LY2109761 improved the therapeutic effect of TAE and inhibited intravasation and metastasis after TAE. Based on the observations herein, we concluded that using LY2109761 and TAE in combination for the treatment of VX2 rabbit liver cancer inhibits tumour growth and metastasis, suggesting that such a combination may provide new a target and strategy for interventional liver cancer therapy.
Indexed as
Identifiers
31105825PMC6511774W2991693123What OpenQuestion holds
Registered trials
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.